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USMLE Step 2 (Subject) / Renal/Genitourinary (Lesson)

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• Hypernatremia Serum sodium > 145 mEq/L. Usually due to free water loss rather than sodium gain. Etiology:1. Hypovolemic hypernatremia- Renal loss – from diuretics, osmotic diuresis (most commonly due to glycosuria in diabetics), renal failure- Extrarenal loss – from diarrhea, diaphoresis, respiratory losses2. Isovolemic hypernatremia- Diabetes insipidus3. Hypervolemic hypernatremia- Excessive infusion of NaCl, Cushing syndrome, primary hyperaldosteronism Clinical features:- Thirst (due to hypertonicity)- Nausea/vomiting, headache, muscle cramps/weakness- Severe: Seizures, altered consciousness, coma Diagnosis: Based on urine osmolality and urine sodium.- Urine osmolality low (< 300 mOsm/kg)→ < 100 mOsm/kg → Central diabetes insipidus→ 100-300 mOsm/kg → Nephrogenic diabetes insipidus- Urine osmolality high (> 600 mOsm/kg)→ Extrarenal losses → Vomiting, diarrhea, nasogastric tube→ Na+ gain → Hypertonic saline- Intermediate values often due to osmotic diuresis Treatment:- Euvolemic: Free water supplementation- Hypovolemic:→ Symptomatic: 0.9% saline until euvolemic, then 5% dextrose→ Asymptomatic: 5% dextrose
• Hyponatremia Serum sodium < 135 mEq/L. Symptoms usually begin when the sodium level falls to < 120 mEq/L. Etiology and classification:1. Hypotonic hyponatremia = "true hyponatremia" – serum osmolality < 280 mOsm/kg.- Hypovolemic→ Low urine sodium (< 10 mEq/L): Implies increased sodium retention by the kidneys to compensate for extrarenal losses (eg, diarrhea, vomiting, diaphoresis, third-spacing, burns, pancreatitis)→ High urine sodium (> 20 mEq/L): Renal salt loss is likely (eg, diuretic excess, decreased aldosterone)- Euvolemic: SIADH, psychogenic polydipsia, hypothyroidism, RTA- Hypervolemic: This is due to water-retaining states. The relative excess of water in relation to sodium results in hyponatremia. E.g., CHF, nephrotic syndrome (renal failure), liver disease2. Isotonic hyponatremia: Hyperlipidemia, paraproteinemia (e.g., multiple myeloma)3. Hypertonic hyponatremia: Hyperglycemia, mannitol, radiocontrast agents Clinical features:- Mild symptoms: Anorexia, nausea, vomiting, headache, muscle cramps- Moderate symptoms: Muscle weakness, lethargy, confusion- Severe symptoms: Seizures, altered consciousness, coma Diagnosis:1. Calculate serum osmolality. Sosm = (2 x serum Na) + (BUN/2.8) + (glucose/18). 2. Assess volume status.3. Measure urine osmolality.4. Urine sodium concentration. Treatment:- Treat hypervolemic and euvolemic etiologies with water restriction ± diuretics.- If hypovolemic, replete volume with normal saline. If severe hyponatremia (Na < 120 mEq/L), consider hypertonic saline.- Chronic hyponatremia (> 72h) should be corrected slowly (< 8 mEq/L/day) in order to prevent central pontine myelinolysis.
• Hyperkalemia Serum potassium > 5 mEq/L. Etiology:- Reduced excretion: acute and chronic kidney disease - Endocrine causes: hypocortisolism, hypoaldosteronism- Type IV renal tubular acidosis- Release from cells: myolysis, tumor lysis, hemolysis- Hemolysis of blood samples- Drugs: potassium-sparing diuretics, ACE inhibitors, angiotensin receptor blockers, NSAIDs, and trimethoprim-sulfamethoxazole- Insulin deficiency, acidosis, drugs (eg, β-blockers) Clinical presentation:- Arrhythmias (e.g., atrioventricular block, ventricular fibrillation)- Muscle weakness, paralysis- Nausea/vomiting, intestinal colic, diarrhea- ↓ deep tendon reflexes Diagnosis:- Confirm hyperkalemia with a repeat blood draw- ECG "Everything gets bigger:" Tall, peaked T waves; P-wave flattening, lengthening of the PR interval; Shortened QT interval; Lengthening of the QRS interval Treatment: For values > 6.5 mEq/L or ECG changes- Calcium gluconate: should be administered first!- Insulin and glucose- Sodium bicarbonate: in acidemic patients- Beta-2-adrenergic agonists - Forced diuresis (loop diuretics with normal saline solution)- Kayexalate (sodium polystyrene sulfonate) to remove potassium from the bodyC Big K (Calcium gluconate, Bicarbonate/Beta-2 agonists, Insulin + Glucose, Kayexalate) For values < 6.5 and no ECG changes:- Discontinue drugs that increase serum potassium- Avoid high-potassium foods- Cation-exchange resins (e.g., sodium polystyrene sulfonate): bind potassium in the gut via the exchange of Na+ for K+- Loop diuretics: promote excretion of potassium and lower total body potassium stores- Intravenous, non potassium containing fluids: normal saline, dextrose 5% in water
• Hypokalemia Serum potassium < 3.5 mEq/L. Etiology:- Transcellular shifts: Insulin, β2-agonists, and alkalosis all cause potassium shift intracellularly.- Diuretics (e.g., loop or thiazide), 1° and 2° hyperaldosteronism, ↓ circulating volume, Bartter and Gitelman syndromes, drugs (e.g., gentamicin, amphotericin B), DKA- Hypomagnesemia- Type I and II renal tubular acidosis- Gastrointestinal loss: vomiting, diarrhea, laxatives (e.g., in bowel preparation prior to medical procedures) Clinical presentation:- Arrhythmias- Fatigue, muscle weakness, cramps, rhabdomyolysis- Hyporeflexia- Paralytic ileus- Paresthesias, ascending paralysis Diagnosis:- Urinary potassium level→ > 20 mEq/L: renal loss→ < 20 mEq/L: extrarenal loss- ECG: T-wave flattening, U waves, ST-segment depression Treatment:- Oral and/or IV potassium repletion. Always retest the K+ levels after administration.- Replace magnesium.
• Hypocalcemia Serum calcium < 8.5 mg/dL. Etiology:- Hypoparathyroidism- Vitamin D deficiency- Pseudohypoparathyroidism (Albright hereditary osteodystrophy): PTH resistance- Hyperphosphatemia- Hypomagnesium- Chelation from citrate found in blood products- Acute necrotizing pancreatitis- Hyperventilation Clinical presentation:- Muscle cramps, dyspnea, tetany, perioral and acral paresthesias (classic symptoms in the transient hypocalcemia in hyperventilation), and convulsions.- Facial spasm elicited from tapping of the facial nerve (Chvostek sign) and carpal spasm after arterial occlusion by a BP cuff (Trousseau sign) are classic findings.- Cardiac manifestations: Arrhythmias, prolonged QT interval on ECG. Diagnosis:- Ionized Ca2+ and PTH are the most useful tests in the diagnosis.- If the patient had a thyroidectomy, review if there was potential damage to the parathyroid glands.- Mg2+ (if low can induce PTH resistance), albumin, 25-OH vitamin D, and 1,25-OH vitamin D levels may be helpful.- Other workup: ECG may show prolonged QT interval. Treatment: - IV calcium gluconate in 50 mL of 5% dextrose infused over 10-20 mins- Magnesium repletion.- For PTH deficiency: Replacement therapy with vitamin D (or calcitriol) plus a high oral calcium intake, thiazide diuretics
• Hypercalcemia Serum calcium > 10.2 mg/dL (corrected for serum albumin). Etiology:- Hyperparathyroidism- Malignancy- Granulomatous disorders- Familial hypocalciuric hypercalcemia- Pharmacologic: Vitamin D intoxication, milk-alkali syndrome, thiazide diuretics, lithium, hyperthyroidism, Paget's disease of the bonePrimary hyperparathyroidism and hypercalcemia of malignancy account for > 90% of cases of hypercalcemia. Serum calcium is typically higher in hypercalcemia of malignancy (> 13 mg/dL), and patients therefore exhibit more severe symptoms! Clinical features:- Bones (osteopenia, fractures, osteitis fibrosa cystica, arthralgias, myalgias)- Stones (kidney stones)- Groans (abdominal pain, nausea and vomiting, peptic ulcer disease, constipation)- Psychiatric overtones (weakness, fatigue, altered mental status)- Polyuria- Cardiac arrhythmias- Muscle weakness, paresis Diagnosis:- Order a total/ionized calcium, albumin, phosphate, PTH.- Other workup: parathyroid hormone-related peptide (PTHrP) if malignancy is suspected, serum protein electrophoresis for multiple myeloma, bone scan to identify lytic lesions, urinary cAMP elevated in primary hyperparathyroidism, vitamin D if granulomatous disease (sarcoidosis, TB) suspected, and ECG (may show a short QT interval). Treatment:- Mild (total calcium < 12 mg/dL): Oral hydration- Severe or symptomatic hypercalcemia (total calcium > 14 mg/dL): → IV hydration with isotonic saline→ Loop diuretics → Bisphosphonates (e.g., zoledronic acid, pamidronate), in cases of excessive bone resorption (e.g., hypercalcemia of malignancy, immobilization)→ Calcitonin- Hypercalcemic crisis (psychosis, fever, coma): IV hydration and forced diuresis 
• Hypomagnesemia Serum magnesium < 1.5 mEq/L. Etiology:- ↓ intake: Malnutrition, malabsorption, short bowel syndrome, TPN (total parental nutrition), PPIs- ↑ loss: Diuretics, diarrhea, vomiting, alcoholism.- Miscellaneous: DKA, pancreatitis Clinical presentation:- Hyperactive reflexes, tetany, paresthesias, irritability, confusion, lethargy, seizures, and arrhythmias. Diagnosis:- Lab results may show concurrent hypocalcemia and hypokalemia.- ECG may show prolonged PR and QT intervals. Treatment:- IV and oral supplements.- Hypokalemia and hypocalcemia will not correct without magnesium correction.
• Acute kidney injury Defined as an abrupt ↓ in renal function leading to the retention of creatinine and BUN. Definition – KDIGO:- Increase in creatinine by ≥0.3 mg/dL within 48 hours OR- Increase in creatinine to ≥1.5 times baseline, which is known or presumed to have occured in the last 7 daysOR- Urine volume ≤0.5 ml/kg/h for 6 hours Etiology:- Prerenal (60%): Hypovolemia (eg, burns, pancreatitis), hypotension (eg, dehydration, sepsis), ↓ cardiac output- Intrinsic (35%): Acute tubular necrosis, glomerulonephritis, vascular disorder (HUS, TTP), tubulointerstitial nephritis- Postrenal (5%): Congenital malformations, stones, tumor, catheter-associated Clinical presentation:1. Kidney injury2. Oliguric phase (generally < 2 weeks)- Complications: fluid retention (pulmonary edema), hyperkalemia, metabolic acidosis, uremia, lethargy, asterixis3. Polyuric phase (~ 3 weeks)- Complications: loss of electrolytes and water (dehydration, hyponatremia, and hypokalemia)4. Recovery phase (up to 2 years) Diagnostics:- Blood test: ↑ BUN and creatinine levels, metabolic acidosis, hyperkalemia, hypocalcemia, and hyperphosphatemia- Urinalysis: Hyaline casts seen in prerenal failure, positive for protein/RBC casts/WBC casts in intrinsic failure- Ultrasound: may reveal urinary tract obstruction and increased kidney size in postrenal AKI Treatment:- Underlying cause- Discontinue nephrotoxic substances- Monitor pH, water, and electrolyte balance- Remove outflow obstructions (urinary catheter)- Order dialysis if symptomatic uremia, intractable acidemia, hyperkalemia, or volume overload develop.
• Chronic kidney disease Defined as > 3 months of GFR < 60 mL/min or kidney damage (structural/functional abnormalities). Etiology:- Diabetes mellitus (most common cause 45%)- Hypertension (30%)- Glomerulonephritis (8%)- Interstitial nephritis, polycystic kidney disease  Clinical presentation:- Generally asymptomatic until GFR is < 30 mL/min- Cardiovascular: Hypertension, CHF, pericarditis (uremic)- GI (due to uremia): Nausea/vomiting, anorexia- Neurologic: Lethargy, somnolence, confusion, peripheral neuropathy, and uremic seizures- Hematologic: Signs of anemia, bleeding (uremia)- Sexual/reproductive: Amenorrhea, infertility, and hyperprolactinemia- Pruritus Diagnosis:- Blood tests: Azotemia (↑ BUN and creatinine), metabolic acidosis, hyperkalemia, anemia, hypocalcemia, hyperphosphatemia, 2° hyperparathyroidism (↓ phosphate excretion; impaired vitamin D production leading to renal osteodystrophy)- Fluid retention (hypertension, edema, CHF, pulmonary edema)- Abnormal hemostasis caused by impaired platelet aggregation- Urinalysis: broad, waxy casts- Ultrasound: shrunken kidneys and fibrotic parenchyma Treatment:- ACEIs/ARBs and hypertension control- Use desmopressin (DDAVP) in cases of abnormal bleeding- EPO analogues for anemia of chronic disease- Oral phosphate binders (calcium acetate) and calcitriol (1,25-OH vitamin D) for renal osteodystrophy- Renal replacement therapy includes hemodialysis, peritoneal dialysis, and renal transplantation- Vaccinate (Pneumococcus every 5 years; influenza annually) Complications: Acquired renal cystic disease in patients undergoing long-term dialysis. Cardiovascular complications are the most common cause of death.
• Nephritic syndrome A disorder of glomerular inflammation, also called glomerulonephritis. Proteinuria may be present but is usually < 1.5 g/day.  History/PE:The classic findings are oliguria, macroscopic/microscopic hematuria (tea- or cola-colored urine), hypertension, and edema (can also present with pulmonary edema). Diagnosis:- UA shows hematuria and possibly mild proteinuria.- Patients have ↓ GFR with elevated BUN and creatinine.- Renal biopsy may be useful for histologic evaluation. Treatment:- Treat hypertension, fluid overload, and uremia with salt and water restriction, diuretics, and if necessary, dialysis.- In some cases, corticosteroids are useful in reducing glomerular inflammation. Causes:- Immune complex: Postinfectious glomerulonephritis, IgA nephropathy, Henoch-Schönlein purpura- Pauci-immune: GPA, microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis- Anti-GBM disease: Goodpasture syndrome, Alport syndrome
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• Nephrotic syndrome Defined as proteinuria (≥ 3.5 g/day), generalized edema, hypoalbuminemia, and hyperlipidemia. Approximately 1/3 of all cases result from systemic diseases such as DM, SLE, or amyloidosis. History/PE:- Presents with generalized edema and foamy urine. In severe cases, dyspnea and ascites may develop.- Patients have ↑ susceptibility to infection as well as hypercoagulable states with an ↑ risk of venous thrombosis and pulmonary embolism (due to loss of antithrombin III, increased platelet aggregation, and changes in protein C and S levels). Diagnosis:- 24-hour urine collection or spot urine (confirmatory tests): Heavy proteinuria (> 3.5 g/24h)- Urine sediment: Proteinuria, lipiduria, fatty casts (hyaline casts with fat globule inclusions and proteins) appear as “Maltese cross” sign under polarized light- Blood chemistry shows ↓ albumin (< 3 g/dL) and hyperlipidemia.- Evaluation should include workup for 2° causes.- Renal biopsy is used to definitively diagnose the underlying etiology. Treatment:- Treat with protein and salt restriction, judicious diuretic therapy, and antihyperlipidemics.- Immunosuppressant medications may be useful for certain etiologies.- ACEIs ↓ proteinuria and diminish the progression of renal disease in patients with renal scarring (especially in diabetics).- Vaccinate with 23-polyvalent pneumococcus vaccine (PPV23), as patients are at ↑ risk of Streptococcus pneumoniae infection. Causes: Minimal-change disease, membranous nephropathy, focal segmental glomerulosclerosis, diabetic nephropathy, lupus nephritis, renal amyloidosis
• Postinfectious glomerulonephritis Cause of nephritic syndrome. Classically associated with recent group A β-hemolytic streptococcal infection, but can be seen with any infection (usually 2-6 weeks prior). History/PE: Oliguria, edema, hypertension, tea- or color-colored urine. Labs/Histology:- Low serum C3, ↑ ASO and anti-DNase titers- Lumpy-dumpy immunofluorescence Treatment: Supportive with diuretics to prevent fluid overload.
• Henoch-Schönlein purpura Cause of nephritic syndrome. Small vessel vasculitis, often seen in childhood. Etiology:- Preceding infection > 75% of cases preceded by viral or bacterial infection 1-3 weeks prior- Most commonly an upper respiratory tract infection caused by group A streptococcus- Drugs (e.g., some antibiotics and antiarrhythmics) and vaccinations (e.g., yellow fever, cholera) Clinical features:- Skin (∼ 100% of cases)→ Symmetrically distributed, raised, erythematous macules or urticarial lesions that coalesce into palpable purpura (non-blanching skin lesions)→ Most common sites: the lower extremities, buttocks, and other areas of pressure or constraint (e.g., from socks or clothing)- Joints (∼ 75% of cases): arthritis/arthralgia, most common in the ankles and knees- Gastrointestinal tract (∼ 60% of cases)→ Colicky abdominal pain (may be severe enough to mimic an acute abdomen)→ Bloody stools or melena→ Nausea/vomiting- Kidneys (∼ 50% of cases): HSP nephritis with signs and symptoms of nephritic syndrome - Other organs:→ Scrotum (e.g., scrotal swelling, pain, and tenderness)→ Central and peripheral nervous system (e.g., headaches, seizures, focal neurologic deficits, ataxia, intracerebral hemorrhage, central and peripheral neuropathy)→ Respiratory tract (e.g., mild interstitial changes, pulmonary hemorrhage) Diagnostics:- ↑ Platelet count- ↑ IgA in serum- Hematuria, often with RBC casts, possibly proteinuria- Biopsy→ Skin: Leukocytoclastic vasculitis with IgA and C3 immune complex deposition (hallmark) in small vessels of the superficial dermis→ Kidney: Renal involvement characterized by mesangial IgA deposition; C3 and fibrin are also frequently present. Treatment: Supportive therapy ± glucocorticoids
• Microscopic polyangiitis Cause of nephritic syndrome. Small vessel vasculitis timilar to GPA. No granulomas. History/PE:Similar to GPA but no nasopharyngeal involvement.  Labs/Histology:p-ANCA. Necrotizing glomerulonephritis. Treatment: Glucocorticoids, cyclophosphamide, or rituximab
• Goodpasture syndrome Cause of nephritic syndrome. Rapidly progressing glomerulonephritis with pulmonary hemorrhage. Peak incidence in men in their mid-20s.  Clinical features:- Hemoptysis- Dyspnea, possible respiratory failure.- No upper respiratory tract involvement. Labs/Histology:Linear anti-GBM deposits on immunofluorescence; iron deficiency anemia; hemosiderin-filled macrophages in sputum; pulmonary infiltrates on CXR. Treatment: Plasma exchange therapy; pulsed steroids. May progress to ESRD.
• Alport syndrome Cause of nephritic syndrome. Hereditary glomerulonephritis. Presents in boys 5-20 years of age. Pathophysiology: Genetic defect of type IV collagen chains (component of the basement membrane of the kidneys, eye, and cochlea) → kidney damage, sensorineural hearing loss, and ocular abnormalities Clinical features:- Often asymptomatic- Initially intermittent gross hematuria- As glomerular damage progresses → symptoms of nephritic syndrome and chronic kidney disease (usually leads to ESRD between the ages of 16 and 35)- Sensorineural hearing loss (∼ 60% of cases)- Ocular findings (lenticonus) (∼ 25% of cases) Diagnostics:- Urinalysis: best initial test, signs of nephritic syndrome (e.g., hematuria, minor proteinuria)- Skin biopsy: confirmatory test, absence of collagen type IV alpha-5 chains - Kidney biopsy→ Light microscopy: mesangial cell proliferation and sclerosis→ Electron microscopy: splitting and alternating thickening and thinning of the glomerular basement membrane (“basket-weave appearance”)→ Immunostaining: absence of collagen type IV alpha-3 and/or alpha-4 chains Treatment: Progresses to renal failure.
• Minimal-change disease The most common cause of nephrotic syndrome in children. Idiopathic etiology; 2° causes include NSAIDs and hematologic malignancies (eg, Hodgkin disease). History/PE:Tendency toward infectious and thrombotic events. Sudden onset of edema. Labs/Histology:Light microscopy appears normal; EM shows effacement of podocyte processes with lipid-laden renal cortices. Treatment: Steroids; excellent prognosis.
• Focal segmental glomerulonephritis The most common cause of nephrotic syndrome in black populations Etiology: Idiopathic, IV drug use (heroin), HIV, obesity, sickle cell disease  Diagnostics:- LM: segmental sclerosis- IM: IgM and C3 inside the sclerotic regions- EM: Effacement of the foot processes Treatment: Prednisone, cytotoxic therapy, ACEIs/ARBs to ↓ proteinuria
• Membranous nephropathy Accounts for ~30% of nephrotic syndromes in adults. Most common cause of nephrotic syndrome white populations. Primary: Autoantibodies to phospholipase A2 receptorSecondary: Associated with solid-tumor malignancies, infections (hepatitis B, hepatitis C, malaria), SLE, drugs (NSAIDs, gold). Labs/Histology:- LM: glomerular capillary loops and basement membrane appear thickened- EM: "Spike and dome" appearance due to granular deposits of IgG and C3 at the basement membrane. Treatment: Prednisone and cytotoxic therapy Complications: Renal vein thrombosis
• Diabetic nephropathy Cause of nephrotic syndrom. Has 2 characteristic forms: diffuse hyalinization and nodular glomerulosclerosi (Kimmelstiel-Wilson lesions). Pathophysiology: chronic hyperglycemia → non-enzymatic glycosylation (NEG) of the basement membrane (protein glycation) → increased permeability and thickening of the basement membrane and stiffening of the efferent arteriole → hyperfiltration (increase in GFR) → increase in intraglomerular pressure → progressive glomerular hypertrophy and increased renal size → worsening of filtration capacity Pathology: Three major histological changes occur:1. Mesangial expansion2. Glomerular basement membrane thickening3. Glomerulosclerosis (later stages): may be diffuse (most common) or pathognomonic nodular glomerulosclerosis (Kimmelstiel-Wilson nodules) Clinical findings:- Often asymptomatic; patients may complain of foamy urine- Progressive diabetic kidney disease with signs of renal failure and risk of uremia (e.g., uremic polyneuropathy)- Arterial hypertension Urine analysis:- Proteinuria: Initially moderately increased albuminuria (microalbuminuria), eventually significantly increased albuminuria (macroalbuminuria): nephrotic syndrome may develop. Treatment: Tight control of blood sugar; ACEIs or ARBs
• Lupus nephritis - Most crucial prognostic factor in SLE- Can be nephritic or nephrotic- Classified as WHO types I-VI. - The severity of renal disease often determines overall prognosis.  History/PE:Proteinuria or RBCs on UA may be found during evaluation of SLE patients. Pathology: classically, immune complex-mediated glomerulonephritis; diffuse proliferative glomerulonephritis is the most common type. Labs/Histology:Mesangial proliferation; subendothelial and/or subepithelial immune complex deposition. Treatment: Prednisone and cytotoxic therapy
• Renal amyloidosis Causes of nephrotic syndrome. 1° (plasma cell dyscrasia) and 2° (infectious or inflammatory) are the most common. History/PE:Patients may have multiple myeloma or a chronic inflammatory disease (eg, rheumatoid arthritis, TB). Labs/Histology:Nodular glomerulosclerosis; EM reveals amyloid fibrills; apple-green birefringence with Congo red stain. Treatment: Prednisone and melphalan. Bone marrow transplantatin may be used for multiple myeloma.
• Membranoproliferative nephropathy Type I: Nephritic/nephrotic syndrome.- Associated with HBV, HCV, cryoglobulinemia, SLE, and subacute bacterial endocarditis.- Labs/Histology: "Tram-track," double-layered basement membrane. Subendothelial and mesangial deposits. Low serum C3.- Treatment: Corticosteroids and cytotoxic agents.  Type II: Nephritic/nephrotic- Often idiopathic- Intramembranous dense deposits. Occurs by way of C3 nephritic factor.- Treatment: same
• Types of nephrolithiasis Calcium oxalate/calcium phosphate:- Frequency: 83%- Etiology: The most common causes are idiopathic hypercalcuria and 1° hyperparathyroidism. Can also see in fat malabsorption (↑ oxalate absorption). Radiopaque.- Calcium oxalate: Dumbbell or cubed-shaped, envelope-shaped- Urinary pH: ↓ pH (calcium oxalate), ↑ pH (calcium phosphate)- Treatment: Hydration, dietary sodium and protein restriction, thiazide diuretics. Do not ↓ calcium intake (can lead to hyperoxaluria and ↑ risk of osteoporosis) Struvite (Mg-NH4-PO4) or "triple phosphate":- Frequency: 9%- Etiology: Associated with urease-producing organisms (eg, Proteus). Form staghorn calculi. Alkaline urine. Radiopaque.- Rectangular prisms, "coffin-lid"- Urinary pH: ↑- Treatment: Hydration; treat UTI if present; surgical removal of staghorn stone Uric acid: - Frequency: 7%- Etiology: Associated with gout, xanthine oxidase deficiency, and high purine turnover states (eg, chemotherapy). Acidic urine (pH <5.5). Radiolucent on plain film, but detectable with CT.- Rhomboid/needle-shaped crystals- Urinary pH: ↓- Treatment: Hydration; alkalinize urine with citrate, which is converted to HCO3- in the liver; dietary purine restriction and allopurinol Cystine:- Frequency: 1%- Etiology: Due to a defect in renal transport of certain amino acids (COLA: cystein, ornithine, lysine, and arginine). Radiopaque. - Hexagonal crystals - ⊕ urinary cyanide nitroprusside test. - Urinary pH: ↓- Treatment: Hydration, dietary sodium restriction, alkalinization of urine, penicillamine
• Autosomal dominant polycystic kidney disease Characterized by the presence of progressive cystic dilation of the renal tubules, as well as by cysts in the spleen, river, and pancreas.  Epidemiology: ∼ 1/1,000 Etiology: Inherited mutation on chromosome 16 (85% of cases) or 4 (15% of cases) with an alteration of polycystin-1 or 2 Clinical features:- Flank or abdominal pain- Recurrent urinary tract infections- Nephrolithiasis- Multiple hepatic cysts (in up to 70% of cases); cysts may also occur in the pancreas, spleen, ovary, and testicles- Signs of arterial hypertension (e.g., morning headaches)- Heart valve defects (particularly mitral valve prolapse)- Left ventricular hypertrophy- Colon diverticula, abdominal or inguinal hernias- Cerebral berry aneurysm (5-20%) Diagnostics:- Positive family history- Physical examination: palpable, bilateral upper abdominal masses that are not tender to touch- Ultrasound: → Enlarged kidneys with multiple cysts of varying sizes (anechoic masses)→ Hepatic, pancreatic, splenic cysts may be visible- Computer tomography (CT)- Evaluate and monitor renal function and blood pressure- Genetic testing Treatment:- Prevent or delay progression to end stage renal disease (ESRD)→ Regular sonographic monitoring and laboratory evaluation of renal function→ Avoid nephrotoxic substances- Early treatment of arterial hypertension: ACE-inhibitors- Genetic counseling- Kidney transplantation is the only curative option 
• Hydronephrosis Dilation of renal calyces. Usually occurs 2° to obstruction of the urinary tract. In pediatric patients, the obstruction is often at the ureteropelvic junction. In adults, it may be due to BPH, neurogenic bladder (diabetes, spinal cord injuries), tumors, aortic aneurysms, or renal calculi. Can also be caused by high-output urinary flow and vesicoureteral reflux. History/PE:May be asymptomatic, or may present with flank/back pain, ↓ urine output, abdominal pain, and UTIs. Diagnosis:- Ultrasonography or CT scan to detect dilation of the renal calyces and/or ureter.- ↑ BUN and creatinine provide evidence of 2° renal failure. Treatment:- Surgically correct any anatomic obstruction; use laser or sound wave lithotripsy if calculi are causing obstruction.- Ureteral stent placement across the obstructed area of the urinary tract and/or percutaneous nephrostomy tube placement to relieve pressure may be appropriate if the urinary outflow is not sufficiently cleared of obstruction. Foley or suprapubic catheters may be required for lower urinary tract obstruction (eg, BPH).
• Scrotal swelling Painless etiologies → hydrocele (remnant of processus vaginalis), varicocele (dilatation of pampiniform plexus).Painful etiologies → epididymitis (STDs, prostatitis), testicular torsion (twisting of the spermatic cord). History/PE:Physical exams reveals "bag of worms" in varicocele, more often in left testicle than right. ⊕ Prehn sign (↓ pain with scrotal elevation) in epididymitis, ⊝ Prehn sign in torsion. Diagnosis:Hydrocele will transilluminate on ultrasonogram, varcicocele will not. Doppler ultrasonography shows normal to ↑ blood flow to testes in epididymitis, ↓ blood flow in torsion. UA and culture will often show Neisseria gonorrhoeae, Escherichia coli, or Chlamydia in epididymitis. Treatment:- Hydrocele: None needed. Does have an ↑ risk of indirect inguinal hernia.- Varicocele: May need surgery if large or symptomatic.- Epididymitis: Antibiotics (tetracycline, fluoroquinolones); NSAIDs- Testicular torsion: Immediate surgery (under 6 hours) to salvage testis. Attempt manual detorsion only if surgery is unavailable or if it will not delay surgery. Orchiopexy of both testes to prevent future torsion.
• Erectile dysfunction Inability to achieve or sustain an erection sufficient in rigidity or duration for sexual intercourse which is present for a minimum of ∼ 6 months. Etiology:- Vascular: hypertension, diabetes mellitus, cardiovascular disease, hyperlipidemia, smoking- Neurogenic: stroke, brain or spinal cord injury, dementia, Parkinson disease, multiple sclerosis- Endocrine: hypogonadism, hyperprolactinemia, thyroid disorders- Medications:→ Antihypertensives (beta-blockers, thiazide diuretics)→ Antidepressants (SSRIs)→ Dopamine antagonists (e.g., antipsychotics)- Iatrogenic: surgery or radiotherapy (radical prostatectomy, pelvic radiation)- Trauma: pelvic fracture and urethral injury- Alcohol abuse- Psychogenic: depression, anxiety (performance-related), trauma from prior experiences, relationship issues, stress Diagnosis: Clinical- ↓ testosterone, ↑ SHBG , ↑ prolactin, ↓ LH, ↓ FSH, ↑ TSH, ↑ fasting glucose or hemoglobin A1C, abnormal lipid profile- Nocturnal penile tumescence measurement (phallography): measurement of spontaneous nightly erections in erectile dysfunction (primarily performed in a sleep laboratory) to differentiate between organic from psychogenic erectile dysfunction. Lack of nocturnal erections suggests an organic etiology (neurogenic or vascular)- Normal testing suggests a psychogenic etiology- Duplex Doppler ultrasound or arteriography to identify suspected arterial inflow or venous leaks after injection of vasodilatory agent Treatment:- Patients with psychological ED may benefit from psychotherapy involving discussion and exercises with the partner.- Oral sidenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis) are phosphodiesterase-5 (PDE5) inhibitors that result in prolonged action of cGMP-mediated smooth muscle relaxation and ↑ blood flow in the corpora cavernosa.- Testosterone is a useful therapy for patients with hypogonadism of testicular or pituitary origin; it is discouraged for patients with normal testosterone levels.- Vacuum pumps, intracavernosal prostaglandin injections, and surgical implantation of semirigid or inflatable penile prostheses are alternatives for patients for whom PDE5 therapy fails.
• Benign prostatic hyperplasia Benign prostatic hyperplasia (BPH) is a non-neoplastic glandular and stromal hyperplasia of the transition zone of the prostate. BPH most commonly occurs in the central (periurethral) zone of the prostate. Epidemiology:- Age: Prevalence of BPH increases with age (∼ 40 % of males > 50 years).- Race: The severity of symptoms of BPH and the size of the prostate are greater in blacks. Clinical features:- Urinary frequency (polyuria and nocturia)- Urinary urgency and urge incontinence- Dysuria- Hesitancy - Straining to urinate- Poor and/or intermittent stream- Prolonged terminal dribbling- Sensation of incomplete voiding- Often gross hematuria- Digital rectal examination (DRE): symmetrically enlarged, smooth (no nodules), firm, nontender prostate with rubbery or elastic texture Diagnosis:- Obtain a UA and urine culture to rule out infection and hematuria.- Prostate specific antigen levels (PSA): Indicated in men with ≥ 10 year life expectancy to identify co-existent prostate cancer, if present - Consider creatinine levels to rule out obstructive uropathy and renal insufficiency.- Potential findings of abdominal ultrasound→ Increased total prostate volume→ Elevated post-void residual urine volume (e.g., > 100 ml)→ Bladder wall thickening→ Hydronephrosis- Maximal urinary flow rate measurement (Uroflowmetry) Treatment:- First-line: alpha-blockers (e.g., tamsulosin, doxazosin, terazosin, alfuzosin) inhibit α1 receptors (α1A receptors) of the bladder neck and the prostatic urethra- 5-alpha-reductase inhibitor (e.g., finasteride, dutasteride) prevent the conversion of testosterone to DHT - Phosphodiesterase type 5 inhibitors (e.g., tadalafil): Indicated in patients with erectile dysfunction- Transuretral resection of the prostate (TURP) or open prostatectomy is appropriate for patients with moderate to severe symptoms/complications (including renal insufficiency, recurrent UTIs, bladder stones).Almost all surgical interventions lead to retrograde ejaculation into the bladder because of anatomical changes!
• Prostate cancer Risk factors:- Advanced age- Positive family history- African-American race- Genetic disposition (BRCA-2, Lynch syndrome) Clinical features:- Early-stage: Typically asymptomatic- Fatigue, loss of appetite → weight loss- Urinary retention- Hematuria: especially blood at the end of the urine stream (terminal hematuria) indicates damage to the vessels of the bladder or prostate by the tumor. - Incontinence- Hydronephrosis- Erectile dysfunction- Metastatic disease→ Bone pain (bone metastasis, especially lumbosacral spine)→ Neurological deficits due to spinal cord compression→ Lymphedema Diagnostics:- Digital rectal examination (DRE): Screening test- ↑ PSA (> 4 ng/mL), ↑ alkaline phosphatase in bone metastases, ↑ prostatic acid phosphatase (PAP)- Ultrasound-guided transrectal biopsy- Tumors are graded by the Gleason histologic system, which sums the scores (from 1-5) of the two most dysplasic samples (10 is the highest grade).- Staging with CT of the abdomen/pelvis and bone scan  Treatment:- Watchful waiting: for elderly patients with low-grade tumors- Radiation therapy: External beam radiation, brachytherapy; ± androgen deprivation therapy (ADT)- Radical prostatectomy- Antiandrogen: Gonadotropin-releasing hormone agonist (e.g., leuprolide) or antagonist (e.g., degarelix) ± antiandrogen (e.g., flutamide) ± bilateral orchiectomy- Disseminated disease: Antiandrogen therapy + chemotherapy with docetaxel + osteoclast inhibitors (e.g., bisphosphonates, denosumab) in bone metastases
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• Bladder cancer Epidemiology:- Peak incidence: 65 years- Cancer sites: Bladder (90%); Renal pelvis (8%); Ureter (esp. the lower ⅓) and urethra (2%)- Histological types: Transitional cell carcinoma (most common); Squamous cell carcinoma Risk factors:- Smoking- Occupational exposure to aniline dye- Chronic inflammation of the urinary tract (e.g., chronic/recurrent UTI, schistosomiasis) - HPV 16 infection- Iatrogenic: pelvic irradiation; cyclophosphamide treatment Clinical features:- Gross hematuria is the most common presenting symptom.- Other urinary syndroms: frequency, urgency, and dysuria Diagnosis:CT urography and cystoscopy are indicated in all patients with gross hematuria and in patients > 35 years with asymptomatic microhematuria.- Cystoscopy with biopsy is diagnostic- Urinalysis: Hematuria (macro- or microscopic)- Cytology: Dysplastic cells- CT urography: Imaging modality of choice to examine the entire urinary tract Treatment:- Low-risk tumor: Transurethral resection of bladder tumor (TURBT) with/without immediate intravesical chemotherapy (mitomycin or gemcitabine) - High-risk tumor: TURBT with adjuvant intravesical BCG or chemotherapy instillation - Muscle invasive tumors with/without positive lymph nodes and M0: Radical cystectomy; construction of a urinary diversion/neobladder; Neoadjuvant chemotherapy alone or concurrent chemoradiation- Metastatic disease: palliative systemic chemotherapy
• Renal cell carcinoma Epidemiology:- 85% of renal cancers in adults - Age of onset: 60-80 years Risk factors- Male gender- Smoking- Obesity- Hypertension- Acquired cystic kidney disease in ESRD- Hereditary factors: Von Hippel-Lindau disease, Tuberous sclerosis Classification: Clear cell, papillary, chromophobe, oncocytic, Bellini duct Clinical features:- Hematuria, flank pain, and a palpable flank mass- Constitutional symptoms: weight loss, fatigue, night sweats, fever- Left-sided varicocele- Anemia- Paraneoplastic syndrome: Hypertension, polycythemia, hypercalcemia Diagnostics:- Best initial test: abdominal CT scan with contrast- Evaluation of metastatic disease: CT/MRI of the thorax Treatment:- Surgical resection → Stage I: cryoablation, thermal ablation, partial nephrectomy, or simple nephrectomy→ Stage II-IV: radical nephrectomy- Immunomodulatory and/or targeted therapy→ Interferon-α (immunotherapy)→ Recombinant cytokines (e.g., interleukin-2)→ Tyrosine kinase inhibitors (e.g., sorafenib, sunitinib, pazopanib)Chemotherapy is not used to treat RCC because tumor cells express MDR-1 (multidrug resistance protein-1).
• Testicular cancer Epidemiology:- Peak incidence: 20-35 years Risk factors:- Cryptorchidism- Contralateral testicular cancer- Klinefelter syndrome, Down syndrome- Subfertility/infertility, hypospadia Clinical features:- Painless enlargement of the testes- Negative transillumination test- Dull lower abdominal or scrotal discomfort Diagnostics:- Testicular ultrasonography- Abdominal/pelvic CT - Tumor markers: alpha fetoprotein (AFP), human chorionic gonadotropin (HCG) Treatment:- Prior to surgery: sperm cryopreservation- Radical orchiectomy to determine histologic type and stage- Adjuvant chemotherapy→ Non-seminoma: BEP (bleomycin + etoposide + cisplatin)→ Seminoma: Radiation therapy Germ cell tumors (95% of all testicular tumors):- Seminoma: ↑ placental ALP (alkaline phosphatase), β-hCG- Yolk sac: ↑ AFP- Choriocarcinoma: ↑ β-hCG- Teratoma: AFP and/or β-hCGNon-germ cell tumors (5% of all testicular tumors):- Leydig cell: Appear after age 4. ↑ testosterone and estrogen- Sertoli cell: More common in older males, ↑ estrogen- Testicular lymphoma: Arises from metastasis to testes 
• Hypovolemia Etiolgoy:- GI loss: Vomiting, nasogastric suction, diarrhea, fistula drainage, etc.- Third-spacing: Ascites, effusions, bowel obstruction, crush injuries, burns- Inadequate intake- Polyuria: Eg, diabetic ketoacidosis- Sepsis- Trauma, open wounds, sequestration of fluid into soft tissue injuries Diagnostics:- Monitor urine output and daily weights. If critically ill, consider placing a Swan-Ganz catheter (to measure CVP and PCWP)- Elevated serum sodium, low urine sodium, and a BUN/Cr ratio of >20:1 suggest hypoperfusion to the kidneys- Increased hematocrit: 3% increase for each liter of deficit Treatment:1. Correct volume deficit- Use bolus to achieve euvolemia. Begin with isotonic solution (lactated Ringer or NS)- Frequent monitoring of HR, BP, urine output, and weight- Maintain urine output at 0.5-1 mL/kg/hr- Bloss loss – replace with crystalloid at a 3:1 ratio2. Maintenance fluid- D51/2NS solution with 20 mEq KCl/L is most common adult maintenance fluid. Dextose is added to inhibit muscle breakdown.- 100/50/20 rule: 100 mL/kg for first 10 kg, 50 mL/kg for next 10 kg, 20 mL/kg for ever 1 kg over 20. Divide total by 24 for hourly rate.- 4/2/1 rule: 4 mL/kg for first 10 kg, 2 mL/kg for next 10 g, 1 mL/kg for every 1 kg over 20.
• Hypervolemia Etiology:- Iatrogenic (parenteral overhydration)- Fluid-retaining states: CHF, nephrotic syndrome, cirrhosis, ESRD Clinical features:- Weight gain- Peripheral edema, ascites, pulmonary edema- Jugular venous distension- Elevated CVP and PCWP- Pulmonary rales- Low hematocrit and albumin concentration Treatment:1. Fluid restriction2. Judicious use of diuretics3. Monitor urine output and daily weights, and consider Swan-Ganz catheter placement depending on condition.
• Respiratory alkalosis ↑ In respiratory rate and/or tidal volume → alveolar hyperventilation → CO2 washout Etiology:- Pain, anxiety, panic attacks- Pulmonary embolism, pneumonia, asthma- Sepsis- Pregnancy – increased serum progesterone levels cause hyperventilation- High altitude- Drug toxicity (theophylline, salicylate toxicity)- Hyperventilation while on mechanical ventilation Clinical presentation:- Symptoms are mostly related to decreased cerebral blood flow (vasoconstriction): lightheadedness, dizziness, anxiety, paresthesias, and perioral numbness- Tetany (indistinguishable from hypocalcemia)→ An increased pH causes hydrogen ions to dissociate from albumin molecules, thereby freeing up the albumin to bind with calcium → decreased levels of ionized calcium- Arrhythmias (in severe cases)
• Respiratory acidosis Defined as a reduced blood pH and PaCO2 > 40 mm Hg. Etiology: Alveolar hypoventilation → CO2 retention- Airway obstruction: COPD exacerbation, bronchial asthma- Respiratory muscle weakness- Myasthenia gravis- CNS depression: Head trauma, post-ictal state- Drug toxicity (opiates, barbiturates, and benzodiazepines) Clinical presentation:- Somnolence, confusion, and myoclonus with asterixis.- Headaches, confusion, and papilledema are signs of acute CO2 retention. Treatment:1. Verify patency of the airway.2. If PaO2 is low (< 60 mm Hg), initiate supplemental oxygen. Caution: In patients who are “CO2 retainers” (e.g., COPD patients), oxygen can exacerbate the respiratory acidosis, so administer oxygen judiciously.- The following situations require intubation:→ Severe acidosis→ PaCO2 > 60 or inability to increase PaO2 with supplemental oxygen→ If patient is obtunded or shows deterioration in mental status→ Impending respiratory fatigue (ensues with prolonged labored breathing)
• Metabolic alkalosis Loss of H+ or ↑ production/ingestion of HCO3- Etiology:- Saline-responsive (urinary chloride normal [< 20 mEq/L])→ Vomiting or nasogastric suction→ Hypovolemia (contraction alkalosis)→ Loop or thiazide diuretics- Saline-resistant (urinary chloride elevated [> 20 mEq/L])→ Hyperaldosteronism→ Cushing syndrome Clinical features:- Volume depletion: Easy fatigability, postural dizziness, muscle cramps- Hypokalemia: Muscle weakness, arrhythmias- Urine chloride: < 20 mEq/L (saline-responsive), > 20 mEq/L (saline-resistant)
• Metabolic acidosis ↑ Production/ingestion of H+ or loss of HCO3- Etiology:- High anion gap metabolic acidosis→ Lactic acidosis: severe tissue hypoxia, liver failure, metformin use → Ketoacidosis: diabetes mellitus, starvation, alcoholism→ Renal insufficiency, uremia→ Accumulation of exogenous organic acids (methanol, ethylene glycol, salicylate toxicity)- Normal anion gap metabolic acidosis→ Renal tubular acidosis→ GI loss of HCO3- (eg, diarrhea, GI fistulas, intestinal stomas) Clinical presentation:- Hyperventilation (deep rhythmic breathing), also known as Kussmaul respiration- Decreased cardiac output and decreased tissue perfusion. Diagnosis:1. Calculate anion gap2. Winter formula: expected PaCO2 = 1.5 (measured HCO3−) + 8 ± 23. Measure anion gap = Na - [Cl + HCO3-]4. Further evaluation for non-anion gap acidosis: Measure urine anion gap = [Urine Na] + [urine K] - [urine Cl]- Positive urine anion gap → renal acidification (e.g., renal tubular acidosis)- Negative urine anion gap → GI loss of bicarbonate (e.g., diarrhea) Treatment:- Sodium bicarbonate is sometimes needed (especially for normal AG acidosis).- Mechanical ventilation may be required if the patient is fatigued from prolonged hyperventilation, especially in DKA.
• Indications for urgent dialysis (AEIOU) Acidosis:- pH < 7.1 refractory to medical therapy Electrolyte abnormalities:- Symptomatic hyperkalemia→ ECG changes or ventricular arrhythmias- Severe hyperkalemia→ Potassium > 6.5 mEq/L refractory to medical therapy Ingestion:- Toxic alcohols (methanol, ethylene glycol)- Salicylate- Lithium- Sodium valproate, carbamazepine Overload- Refractory fluid overload Uremia- Encephalopathy- Pericarditis- Bleeding
• Proteinuria Proteinuria = urinary protein excretion of > 150 mg/day Diagnosis: Urinalysis- First morning urine→ Elevated protein/creatinine → Evaluate for glomerular/parenchymal disease→ Normal protein/creatinine, ⊕ protein on subsequent urinalysis → Orthostatic proteinuria→ Normal protein/creatinine, Θ protein on subsequent urinalysis → Transient proteinuria- 24-hour urine collection or urine protein-to-creatinine ratio in a spot urine sample to rule out orthostatic proteinuria- Urine sediment to rule out glomerular disease- Electrophoresis to rule out tubulointerstitial diseases and multiple myeloma Microalbuminuria = Urine albumin excretion of 30-300 mg/day- Diagnosis is made if two out of three tests are positive. - Early symptom of diabetic and hypertensive nephropathy Overt proteinuria (formerly "macroalbuminuria"): Urine albumin excretion > 300 mg/day Origin:- Glomerular→ Loss of negative charge of glomerular basement membrane: Only small-to medium-sized proteins can be found in the urine (primarily albumin)→ Damage to the glomerular basement membrane: All types of protein of any size can be found in the urine (albumin, transferrin, and IgG are commonly detected)- Tubular → Damage to the tubules → failure to reabsorb small proteins in the tubules → urinary protein excretion→ The detection of beta-2 microglobulin without large proteins is typical.- Overflow proteinuria→ Increased production of low-molecular-weight proteins → The reabsorption capacity of the tubules is exceeded.→ Light chains or Bence-Jones protein (see myeloma kidney)→ Hemoglobinuria (in hemolysis)→ Myoglobinuria (in rhabdomyolysis)- Post-renal proteinuria→ Proteins that are being produced in the tubules (Tamm-Horsfall protein) Benign proteinuria = Isolated proteinuria < 3.5 g/day- Orthostatic proteinuria (postural proteinuria): increased protein excretion only in the upright position- Transient proteinuria- A dipstick test should be repeated to exclude underlying disease.- No treatment necessary; excellent prognosis
• Hematuria Microhematuria: hematuria that is not grossly visibleMacrohematuria: hematuria that is grossly visible  Urinalysis: - > 3 erythrocytes/HPF or > 5 erythrocytes/μL- If normal → evaluate for coagulation disorders, kidney stones, and malignancy (see bladder cancer)- If pyuria → urine culture (see urinary tract infection)- If RBC casts and proteinuria → evaluate for glomerular diseases Differential diagnosis:- Nephritic syndrome- Infection: Cystitis, urethritis, prostatitis- If asymptomatic, consider malignancy: Urothelial cancer, renal cell carcinoma, prostate cancer- In children, Wilms tumor- Urolithiasis- Coagulation disorder (e.g., hemophilia)- Polycystic kidney disease- Myoglobinuria in professional athletes or crush syndrome- Medication side effect- Porphyrias
• Acute interstitial nephritis Etiology:- Antibiotics, NSAIDs, diuretics, allopurinol, PPIs, phenytoin Pathophysiology: Drugs, particularly antibiotics and NSAIDs, act as haptens, inducing a hypersensitivity reaction. Symptoms:- Painless hematuria- Flank pain- Sterile pyuria- Peripheral eosinophilia- Rash- Fever- Arthralgias Diagnostics:- Pyuria, Eosinophiluria Treatment: Discontinue drugs and administer IV fluids.
• Renal papillary necrosis Coagulative necrosis of the renal medullary pyramids and papillae Etiology:- Pyelonephritis- Obstruction of the urinary tract- Sickle cell disease - Analgesic abuse: due to inhibition of prostaglandin-mediated vasodilation in the vasa recta- Renal transplant rejection- Diabetes mellitus Clinical features (can be acute or chronic):- Patients with a chronic course are usually asymptomatic or only present with mild symptoms- Flank pain, colicky pain- Hematuria (microscopic or macroscopic)- Fever, chills- Acute kidney injury (rare) Treatment: Treat the underlying cause, and stop the offending agents (e.g., NSAIDs).
• Type 4 renal tubular acidosis Pathophysiology: aldosterone deficiency and/or resistance Etiology:- Primary adrenal insufficiency (Addison's disease)- Diabetic nephropathy- SLE- Drugs: NSAIDs, ACE inhibitors, heparin, cyclosporin, potassium-sparing diuretics (e.g., spironolactone, amioloride, eplerenone), TMX Clinical features:- Polyuria → polydipsia, dehydration Diagnostics:- Non-anion gap metabolic acidosis- Hyperkalemia- Urine pH < 5.5 Treatment: - Furosemide- Mineralocorticoid replacement (fludrocortisone)- Low-potassium diet
• Autosomal recessive polycystic kidney disease Epidemiology: ∼ 1/20,000 Etiology: Inherited mutation on chromosome 6 Clinical features:- Chronic renal failure: frequently hematuria, proteinuria- Protruding abdomen due to renal enlargement or hepatomegaly- Severe in-utero renal impairment → maternal oligohydramnios → Potter sequence→ Craniofacial abnormalities (retrognathia, low-set ears, flat nose) and clubbed feet→ Pulmonary hypoplasia → respiratory insufficiency in neonates- Obligate liver involvement: portal fibrosis → portal hypertension and progressive liver failure- Hypertension Diagnostics:- Positive family history- Physical examination: palpable, bilateral upper abdominal masses that are not tender to touch- Ultrasound:→ Enlarged kidneys; diffuse increased echogenicity despite the presence of liquid-filled cysts (anechoic)→ Hepatic cysts; fibrosis- Computer tomography (CT)- Evaluate and monitor renal function and blood pressure- Liver biopsy in ambiguous cases- Genetic testing Treatment:- Prevent or delay progression to end stage renal disease (ESRD)→ Regular sonographic monitoring and laboratory evaluation of renal function→ Avoid nephrotoxic substances- Early treatment of arterial hypertension: ACE-inhibitors - Monitor and treat liver failure- Genetic counseling- Kidney transplantation is the only curative option
• Renal artery stenosis Etiology:- Atherosclerosis (∼ 90% of cases): occurs more often in men > 50 years of age- Fibromuscular dysplasia (∼ 10% of cases): mostly affects women < 50 years of age- Post-transplantation Clinical features:- Abdominal bruits heard over the flank or epigastrium; present during both systole and diastole- Hypertension that is often resistant to therapy (uncontrolled despite 3-drug regimen)- Malingant hypertension (with end-organ damage)- Onset of severe hypertension (> 180/120 mmHg) after age 55- Severe hypertension with diffuse atherosclerosis- Recurrent flash pulmonary edema with severe hypertension- Features of renal insufficiency (e.g., nausea, edema) Diagnostics:- Labs: ↑ Serum creatinine > 30% after antihypertensive treatment with ACE inhibitors or angiotensin-receptor blockers is a strong indication of renal artery stenosis; hypokalemia- Imaging (confirmatory test): First-line: Duplex ultrasonography OR CT or MR angiography- Findings: → Tubular stenosis of the proximal renal artery segment → typically atherosclerotic disease→ Stenosis of the distal renal artery segment with a “string-of-beads” appearance → typically fibromuscular dysplasia→ Significant renal artery stenosis: > 60% reduction in the diameter of the renal artery→ Increased systolic flow velocity in the renal artery (Duplex) → Asymmetric renal size (> 1.5 cm) Treatment:- Patients with atherosclerosis: reduce risk factors by statin therapy and lifestyle modification- Antihypertensive therapy: ACE inhibitors, angiotensin receptor blockers, calcium channel blocker, beta blockers - Percutaneous transluminal renal angioplasty (Atherosclerotic disease: with stenting; Fibromuscular dysplasia: typically without stenting)
• Nephrolithiasis - Classification Calcium oxalate stones (most common, ∼ 80%)- Etiology: Hypercalciuria, hyperoxaluria, hypocitraturia- Urinary pH ↓- Treatment: Dietary modification, urine alkalinization, thiazide diuretics Calcium phosphate stones:- Etiology: Hyperparathyroidism, hypocitraturia (due to type 1 renal tubular acidosis)- Urinary pH ↑ - Treatment: Urine acidification Uric acid stones: ∼ 10%- Etiology: Persistently acidic urine; gout, hyperuricemia and hyperuricosuria- Urinary pH ↓ - Treatment: Low-purine diet, urine alkalinization Struvite stones (staghorn stones): ∼ 5–10%- Etiology: UTIs with urease-producing bacteria such as Proteus mirabilis, Klebsiella, Pseudomonas, Providencia, Enterobacter, and Ureaplasma urealyticum; Use of indwelling catheter- Urinary pH ↑ - Treatment: Treatment of urinary tract infections; urine acidification; usually require surgical stone removal Cysteine stones: ∼ 1%- Etiology: Cystinuria (Autosomal recessive disorder characterized by defective intestinal or renal tubular transport of COAL – cystine, ornithine, arginine, lysine)- Diagnosis: Nitroprusside probe (cyanide nitroprusside test).- Urinary pH ↓ - Treatment: Urine alkalinization
• Nephrolithiasis Clinical features:- Severe unilateral and colicky flank pain (renal colic)- Radiates anteriorly to the lower abdomen, groin, labia, testicles, or perineum - Paroxysmal or progressively worsening- The area around the kidneys may be tender on percussion- Hematuria- Nausea, vomiting, and reduced bowel sounds- Dysuria, frequency, and urgency Diagnostics:- ↑ Serum urea nitrogen and creatinine: suggests acute kidney injury- Urine dipstick and urinalysis: Gross or microscopic hematuria→ Pyuria, positive leukocyte esterase, positive nitrites, or bacteriuria (suggests UTI)→ Urine pH > 7 suggests urea-splitting organisms and struvite stones→ < 5 indicates uric acid stones- Urine microscopy: may detect crystals→ Dumbbell-shaped or cube-shaped crystals indicate calcium oxalate stones→ Rhomboid/needle-shaped crystals indicate uric acid stones→ Rectangular prisms (coffin lid-appearance) indicate struvite stones- Urine culture: obtain in patients with clinical or laboratory signs of UTI- Straining of urine: enables chemical analysis of stone composition and specific guidance on preventive treatment - 6 weeks later: Twenty-four–hour urine: collect to assess Cr, calcium, uric acid, oxalate, and citrate levelsImaging:- Nonenhanced abdominopelvic CT scan (Gold standard) - Ultrasound: method of choice for patients in whom radiation exposure should be minimized (e.g., pregnant patients, children, recurrent stone formers)   Treatment:- Uncomplicated stones ≤ 10 mm: offer observation with symptomatic treatment = Hydration; analgesia (NSAIDs, IV morphine), alpha blockers (eg, tamsulosin) or calcium channel blockers (eg, nifedipine)- Uric acid stones: dissolve with urine alkalinization- Urological intervention:→ Stones > 10 mm→ Complicated stones, i.e., concomitant high-grade obstruction, urosepsis, impending acute kidney injury, intractable pain vomiting→ After failed medical therapy, relapse, recurrent infection, or if preferred by patient→ Stones ≤ 20 mm: Ureterorenoscopy and shock wave lithotripsy→ Stones > 20 mm: Percutaneous nephrolithotomy 
• Renal mass - Differential Benign masses:- Angiomyolipoma- Oncocytoma- Metanephric adenoma- Renal abscess- Granulomatous renal disease (e.g., renal tuberculosis, xanthogranulomatous pyelonephritis)- Renal cysts (e.g., polycystic kidney disease) Malignant masses:- Renal cell carcinoma- Transitional cell/urothelial carcinoma of the renal pelvis (∼ 8% of renal tumors)- Metastasis from extrarenal tumors- Other rare primary malignancies: lymphomas, soft tissue sarcomas, carcinoid tumors

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