Nephroblastoma (Wilms tumor)
Most common renal malignancy of early childhood (ages 2-4). Contains embryonic glomerular structures. - Presents with large, palpable, unilateral flank mass and/or hematuria. - Loss of function mutation of tumor suppressor genes WT1 (encodes a zink finger transcription factor) or WT2 on chromosome 11. May be part of several symptoms:- WAGR complex: Wilms tumor, Aniridia, Genitourinary malformations, mental Retardation (WT1 deletion)- Denys-Drash syndrome – Wilms tumor, diffuse mesangial sclerosis (early-onset nephrotic syndrome), male pseudohermaphroditism, WT1 mutation- Beckwith-Wiedemann syndrome – Wilms tumor, macroglossia, organomegaly, hemihyperplasia (WT2 mutation)
Transitional cell carcinoma
Also known as urothelial carcinoma.Most common tumor of urinary tract system (can occur in renal calyces, renal pelvis, ureters, and bladder). - Can be suggested by painless hematuria (no casts). Associated with:- Phenacetin (banned analgesic)- Smoking- Aniline dyes (textile industry)- Cyclophosphamide
Autosomal dominant polycystic kidney disease
Numerous cysts in cortex and medulla causing bilateral enlarged kidneys ultimately destroy kidney parenchyma - Presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure - Mutation in PKD1/2 - Death from complications of chronic kidney disease or hypertension (caused by ↑ renin production) - Associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts Treatment: ACE inhibitors or ARBs
Potter's sequence (syndrome)
Oligohydramnios → compression of developing fetus → limb deformities, facial deformities (eg, low-set ears and retrognathia, flattened nose), compression of chest and lack of amnionic fluid aspiration into fetal lungs → pulmonary hypoplasia (cause of death). - Cause includes ARPKD, obstructive uropathy (eg, posterior urethral valves), bilateral renal agenesis, chronic placental insufficiency.
Horseshoe kidney
- Inferior poles of both kidneys fuse abnormally. - As they ascend form pelvis during fetal development, horseshoe kidneys get trapped under inferior mesenteric artery and remain low in the abdomen. - Kidneys function normally. - Associated with hydronephrosis (eg, ureteropelvic junction obstruction), renal stones, infection, chromosomal aneuploidy syndromes (eg, Turner syndrome; trisomies 13, 18, 21), and rarely renal cancer.
Course of ureters
Course of ureter: arises from renal pelvis, travels under gonadal arteries → over common iliac artery → under uterine artery/vas deferens (retroperitoneal). Gynecologic procedures (eg, ligation of uterine or ovarian vessels) may damage ureter → ureteral obstruction or leak. Muscle fibers within the intramural part of the ureter prevent urine reflux. 3 constrictions of ureter:- Ureteropelvic junction- Pelvic inlet- Ureterovesical junction
Changes in glomerular dynamics
Afferent arteriole constriction: ↓ RPF, ↓ GFR, FF unchanged Efferent arteriole constriction: ↓ RPF, ↑ GFR, FF ↑ ↑ plasma protein concentration: RPF unchanged, GFR ↓, FF ↓ ↓ plasma protein concentration: RPF unchanged, GFR ↑, FF ↑ Constriction of ureter: RPF unchanged, ↓ GFR, FF ↓ Dehydration: ↓↓ RPF, ↓ GFR, FF ↑
Amino acid clearance
Sodium-dependent transporters in proximal tubule reabsorb amino acids. Hartnup's disease = dificiency of neutral amino acid (tryptophan) transporter; results in pellagra (the 3 D's: Dermatitis, Diarrhea, Dementia)
Prostaglandins
Paracrine secretion vasodilates the afferent arterioles to ↑ GFR
Potassium shifts
Shifts K+ out of cell (causing hyperkalemia)- Digitalis- Hyper-osmolarity- Lysis of cells (eg, crush injury, rhabdomyolysis, tumor lysis syndrome)- High blood surgar (insulin deficieny)- Acidosis- β-blockers- Succinylcholine (↑ risk in burns/muscle trauma) Shifts K+ into cell (causing hypokalemia)- Hypo-osmolarity- Insulin (↑ Na+/K+ ATPase)- Alkalosis- β-adrenergic agonist (↑ Na+/K+ ATPase)
Electrolyte disturbances
Na+- Low serum concentration: Nausea and malaise, stupor, coma- High serum concentration: Irritability, stupor, coma K+- Low serum concentration: U waves and flattened T waves on ECG, arrhythmias, muscle cramps, spasm, weakness- High serum concentration: Wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness Ca2+- Low serum concentration: Tetany, seizures, QT prolongation, twitching (Chvostek sign), spasm (Trousseau sign)- High serum concentration: Stones (renal), bones (pain), groans (abdominal pain), thrones (↑ urinary frequency), psychiatric overtones (anxiety, altered mental status) Mg2+- Low serum concentration: Tetany, torsades de pointes, hypokalemia, hypocalcemia (when [Mg2+] <1.2 mg/dL)- High serum concentration: ↓ DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalemia PO43-- Low serum concentration: Bone loss, osteomalacia (adults), rickets (children)- High serum concentration: Renal stones, metastatic calcifications, hypocalcemia
↑ anion gap
MUDPILES:MethanolUremiaDiabetic ketoacidosisPropylene glycolIron tablets Lactic acidosisEthylene glycolSalicylate
Normal anion gap (8-12 mEq/L)
HARD-ASS:HyperalimentationAddison's diseaseRenal tubular acidosisDiarrheaAcetazolamideSpironolactoneSaline infusion
Renal tubular acidosis (RTA)
Type 1 ("distal"): Inability of α-intercalated cells to secrete H+ → no new HCO3- is generated → metabolic acidosis.- Urine pH >5.5.- Serum K+ ↓- Causes: Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, autoimmune disease (eg, SLE)- ↑ risk for calcium phosphate kidney stones (due to ↑ urine pH and ↑ bone turnover) Type 2 ("proximal"): Defect in proximal tubule HCO3- reabsorption → ↑ excretion of HCO3- in urine → metabolic acidosis- Urine can be acidified by α-intercalated cells in collecting duct, but not enough to overcome the increased excretion of HCO3- → metabolic acidosis- Urine pH <5.5- Serum K+ ↓- Causes: Fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors- ↑ risk for hypophosphatemic rickets (in Fanconi syndrome) Type 4: Hyperkalemic renal tubular acidosis:- Hypoaldosteronism or aldosterone resistance → hyperkalemia → ↓ NH3 synthesis in PCT → ↓ NH4 secretion- Urine pH <5.5- Serum K+ ↑- Causes: ↓ aldosterone production (eg, diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance (eg, K+-sparing diuretics, nephropathy due to obstruction, TMP-SMX).
Glomerular diseases
Nephritic syndrome: Due to GBM disruption. Hypertension, ↑ BUN and creatinine, oliguria, hematuria, RBC casts in urine. Proteinuria often in the subnephrotic range (<3.5 g/day) but in severe cases may be in nephrotic range.- Acute poststreptococcal glomerulonephritis- Rapidly progressive glomerulonephritis- IgA nephropathy (Berger disease)- Alport syndrome Nephrotic syndrome: Podocyte disruption → change barrier impaired. Massive proteinuria (>3.5 g/day) with hypoalbuminemia, hyperlipidemia, edema.- Focal segmental glomerulosclerosis (1° or 2°)- Membranous nephropathy (1° or 2°)- Minimal change disease (1° or 2°)- Amyloidosis (2°)- Diabetic glomerulonephropathy (2°) Nephritic-nephrotic syndrome: Severe nephritic syndrome with profound GBM damage that damages the glomerular filtration charge barrier → nephrotic-range proteinuria (>3.5 g/day) and comitant features of nephrotic syndrome. Can occur with any form of nephritic syndrome, but is most commonly seen with:- Diffuse proliferative glomerulonephritis- Membranoproliferative glomerulonephritis
Nephrotic syndrome
Massive proteinuria (>3.5 g/day) with hypoalbuminemia, resulting edema, hyperlipidemia. Frothy urine with fatty casts.- Disruption of glomerular filtration charge barrier may be 1° (eg, direct sclerosis of podocytes) or 2° (systemic process [eg, diabetes] secondarily damages podocytes).- Severe nephritic syndrome may present with nephrotic syndrome features if damage to GBM is severe enough to damage charge barrier.- Associated with hypercoagulable state due to antithrombin (AT) III loss in urine and ↑ of infection (loss of immunoglobulins in urine and soft tissue compromise by edema). - Focal segmental glomerulosclerosis- Membranous nephropathy- Minimal change disease (lipoid nephrosis)- Amyloidosis- Diabetic glomerulonephropathy
Focal segmental glomerulosclerosis
- Most common cause of nephrotic syndrome in African Americans and Hispanics.- Can be 1° (idiopathic) or 2° to other conditions (eg, HIV infection, sickle cell disease, heroin abuse, massive obesity, interferon treatment, or congenital malformations).- 1° disease has inconsistent response to steroids. May progress to CKD. LM – Segmental sclerosis and hyalinosis. Some glomeruli are collapsed. The sclerotic segments feature basement membrane collapse, increased matrix production, and hyalinosis.IF – Often Θ but may be ⊕ for nonspecific focal deposits of IgM, C3, C1.EM – Effacement of foot process similar to minimal change disease. - One variant of FSGS with a particularly poor prognosis is collapsing glomerulopathy, which is considered characteristic of HIV-associated nephropathy. The usual FSGS lesions are seen in addition to the collapse and sclerosis of the whole glomerular tuft. The glomerular epithelial cells tend to proliferate and hypertrophy, and marked tubular injury with accompanying microcyst formation is seen.
Membranous nephropathy
- Most common cause of 1° nephrotic syndrom in Caucasian adults.- Can be 1° (eg, antibodies to phospholipase A2 receptor) or 2° to drugs (eg, NSAIDs, penicillamine, gold), infections (eg, HBV, HCV), SLE, or solid tumors.- 1° disease has poor response to steroids. May progress to CKD. LM – Diffuse capillary and GBM thickening.IF – Granular due to IC deposition. SLE's nephrotic presentation.EM - "Spike and dome" appearance of subepithelial deposits.
Minimal change disease (lipoid nephrosis)
- Most common cause of nephrotic syndrome in children.- Often 1° (idiopathic) and may be triggered by a recent infection, immunization, immune stimulus, insect sting/bite.- Rarely, may be 2° to lymphoma (eg, cytokine-mediated damage). Immune dysfunciton leads to overproduction of glomerular permeability factor, a cytokine that directly damages podocytes (causing foot process effacement and fusion) that decreases the anionic properties of the glomerular basement membrane. Loss of negative charge leads to selective loss of albumin in the urine (selective albuminuria). - 1° disease has excellent response to corticosteroids. LM – Normal glomeruli (lipid may be seen in PCT cells).IF – ΘEM – Effacement of podocyte foot processes
Amyloidosis
Kidney is the most commonly involved organ (systemic amyloidosis). - Associated with chronic conditions that predispose to amyloid deposition (eg, AL amyloid, AA amyloid). LM – Congo red stain shows apple-green birefringence under polarized light due to amyloid deposition in the mesangium.
Membranoproliferative glomerulonephritis
MPGN is a nephritic syndrom that often co-presents with nephrotic syndrome.- Mostly affects young individuals. Type I may be 2° to hepatitis C > B infection. May also be idiopathic.- Subendothelial IC deposits with granular IF. Type II is associated with C3 nephritic factor (IgG antibody that stabilizes C3 convertase → persistent complement activation → ↓ C3 levels).- Intramembranous deposits also called dense deposit disease. - In both types, mesangial ingrowth → GBM splitting → "tram-track" appearance on H&E and PAS stains.- Enlarged, hypercellular glomeruli accompanied by infiltration of neutrophils and monocytes.
Diabetic glomerulonephropathy
Most common cause of ESRD in the United States. - Hyperglycemia → nonenzymatic glycosylation of tissue proteins → mesangial expansion; GBM thickening and ↑ permeability. - Hyperfiltration (glomerular HTN and ↑ GFR) → glomerular hypertrophy and glomerular scarring (glomerulosclerosis) leading to further progression of nephropathy. LM - mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesion)
Nephitic syndrome
Inflammatory process. When it involves glomeruli, it leads to hematuria and RBC casts in urine. - Associated with azotemia, oliguria, hypertension (due to salt restriction), and proteinuria (<3.5 g/d) - Acute poststreptococcal glomerulonephritis- Rapidly progressive (crescentic) glomerulonephritis- Diffuse proliferative glomerulonephritis- Berger's disease (IgA nephropathy)- Alport syndrome
Alport syndrome
Mutation in type IV collagen → thinning and splitting of basement membrane.- X-linked dominant - Glomerulonephritis (EM – "Basket weave" appearance)- Sensorineural deafness- Eye problems (eg, retinopathy, lens dislocation)
IgA nephropathy (Berger disease)
Episodic hematuria that occurs concurrently with respiratory or GI tract infections (IgA is secreted by mucosal linings). Renal pathology of IgA vasculitis (Henoch-Schönlein purpura). LM – Mesangial proliferationIF – IgA-based IC deposits in mesangiumEM – Mesangial IC deposition
Diffuse proliferative glomerulonephritis (DPGN)
Often due to SLE. DPGN and MPGN often present as nephrotic syndrome and nephritic syndrome concurrently. LM – "Wire looping" of capillariesIF – GranularEM - Subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition
Rapidly progressive (crescentic) glomerulonephritis
Poor prognosis, rapidly deteriorating renal function (days to weeks).- LM – Crescent-moon shape. Crescents consist of fibrin and plasma proteins (eg, C3b) with glomerular parietal cells, monocytes, and macrophages. Several disease processes may result in this pattern which may be delineated via IF pattern.- Linear IF due to antibodies to GBM and alveolar basement membrane: Goodpasture syndrome – hematuria/hemoptysis; type II hypersensitivity reaction. Treatment: plasmapheresis.- Negative IF/Pauci-immune (no Ig/C3 deposition):Granulomatosis with polyangiitis (Wegener) – PR3/ANCA/c-ANCA or Microscopic polyangiitis – MPO-ANCA/p-ANCA- Granular IF – PSGN or DPGN
Acute poststreptococcal glomerulonephritis
- Most frequently seen in children.- ~2-4 weeks after group A streptococcal infection of pharynx or skin.- Resolves spontaneously in most children; may progress to renal insufficiency in adults.- Type III hypersensitivity reaction.- Presents with peripheral and periorbital edema, cola-colored urine, hypertension.- ⊕ strep titers/serologies, ↓ C3 levels due to consumption. LM – Glomeruli enlarged and hypercellular, neutrophilsIF – "starry sky" granular appearance, "lumpy-dumpy" appearance due to IgG, IgM, and C3 deposition along GBM and mesangiumEM – subepithelial immune complex (IC) humps
Kidney stones - Uric acid
About 5% of all stones. - Risk factors: ↓ urine volume, arid climates, acidic pH.- Strong association with hyperuricemia (eg, gout). Often seen in diseases with ↑ cell turnover, (eg, leukemia). - Precipitates at ↓ pH- X-ray findings: Radiolucent- Minimaly visible on CT and ultrasound- Rhomboid or rosettes Treatment: alkalinization of urine, allopurinol.
Kidney stones - Calcium
Calcium stones most common (80%); calcium oxalate > calcium phosphate Calcium oxalate:- Precipitates with hypocitraturia (eg, distal RTA). Hypocitraturia often associated with ↓ urine pH. - Can result from ethylene glycol (antifreeze) ingestion, vitamin C abuse, hypocitraturia, hypercalciuria (eg, hyperthyroidism), hyperoxaluria (eg, malabsorption in Crohn disease), diet: ↑ sodium, ↑ protein, ↑ oxalate, ↓ calcium.- X-ray findings: Radiopaque- CT findings: Radiopaque- Shaped like envelope or dumbbellTreatment: thiazides, citrate, low-sodium diet. Calcium phosphate: - Precipitates with ↑ pH.- Seen in renal tubular acidosis type I (distal)- X-ray findings: Radiopaque- CT findings: Radiopaque- Wedge-shaped prismTreatment: low-sodium diet, thiazides.
Kidney stones - Ammonium magnesium phosphate
Also known as struvite; account for 15% of stones. - Caused by infection with urease ⊕ bugs (eg, Proteus mirabilis, Staphylococcus saphrophyticus, Klebsiella) that hydrolyze urea to ammonia → urine alkalinization. - Commonly form staghorn calculi. - Precipitate with ↑ urine pH- X-ray findings: Radiopaque- CT findings: Radiopaque- Coffin lid
Kidney stones - Cystine
Hereditary (autosomal recessive) condition in which cystine-resorbing PCT transporter loses function, causing cystinuria. Transporter defect also results in poor absorption of ornithine, lysine, arginine. Cystine is poorly soluble, thus stones form in urine.- Usually begins in childhood.- Can form staghorn calculi.- Sodium cyanide nitroprusside test ⊕. - Precipitates at ↓ pH- X-ray findings: faintly radiopaque- CT findings: moderately radiopaque- Hexagonal crystals Treatment: low sodium diet, alkalinization of urine, chelating agents if refractory.
Renal cell carcinoma
Polygonal clear cells filled with accumulated lipids and carbohydrates. Often golden-yellow due to ↑ lipid content.Originated from PCT → invades renal vein (may develop varicocele if left sided) → IVC → hematogenous spread → metastasis to lung ("cannonball metastases") and bone (osteolytic).- Most common 1° renal malignancy.- Most common in men 50-70 years of age, ↑ incidence with smoking and obesity.- Associated with gene deletion on chromosome 3p (sporadic, or inherited as von Hippel-Lindau syndrome). - Manifests with hematuria, palpable masses, 2° polycythemia, flank pain, fever, and weight loss.- Associated with paraneoplastic syndromes, eg, ectopic EPO, ACTH, PTHrP, renin). Histopathology: Rounded polygonal or cuboidal cells. Abundant clear or yellow cytoplasm. Treatment: surgery/ablation for localized disease. Immunotherapy (eg, aldesleukin) or targeted therapy for metastatic disease, rarely curative.- Resistant to chemotherapy and radiation therapy.
Pyelonephritis
Acute:- Neutrophils infiltrate renal interstitium.- Affects cortex with relative sparing of glomeruli/vessels.- Presents with fever, flank pain (costovertebral angle tenderness), nausea/vomiting, chills.- Causes include ascending UTI (E coli is most common), hematogenous spread to kidney.- Presents with WBCs in urine ± WBC casts - CT would show striated parenchymal enhancement.- Risk factors include indwelling urinary catheter, urinary tract obstruction, vesicourethral reflux, diabetes mellitus, pregnancy.- Complications include chronic pyelonephritis, renal papillary necrosis, perinephric abscess, urosepsis. Chronic:- The result of recurrent episodes of acute pyelonephritis.- Typically requires predisposition to infection such as vesicourethral reflux or chronically obstructing kidney stones.- Coarse, asymmetric corticomedullary scarring, blunted calyx. - Tubules can contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney).Xanthogranulomatous pyelonephritis – rare; grossly orange nodules that can mimic tumor nodules; characterized by widespread kidney damage due to granulomatous tissue containing foamy macrophages. Associated with Proteus infection.
Acute interstitial nephritis (tubulointerstitial nephritis)
Acute interstitial renal inflammation.Pyuria (classically eosinophils) and azotemia occuring after administration of drugs that act as haptens, inducing hypersensitivity. - Nephritis typically occurs 1-2 weeks after certain drugs, but can occur months after starting NSAIDs. Causes:- Most commonly caused by a hypersensitivity reaction to drugs- Drugs: diuretics, penicillin derivates, sulfonamides, rifampin, PPIs, NSAIDs- Autoimmune diseases (eg, Sjögren syndrome, SLE, sarcoidosis)- Systemic infections (eg, Mycoplasma, Legionella) - Associated with fever, rash, and costovertebral angle tenderness, but can be asymptomatic. Laboratory findings:- Acute kidney injury- Pyuria, hematuria, WBC casts- Eosinophilia, urinary eosinophils- Biopsy: Inflammatory interstitial infiltrate (T lymphocytes, monocytes) and edema
Diffuse cortical necrosis
Acute generalized cortical infarction of both kidneys. - Likely due to a combination of vasospasm and DIC. - Associated with obstetric catastrophes (eg, abruptio placentae), septic shock.
Acute kidney injury
Formerly known as acute renal failure. Acute kidney injury is defined as an abrupt decline in renal function as measured by ↑ creatinine and ↑ BUN or by oliguria/anuria. Prerenal azotemia: Due to ↓ RBF (eg, hypotension) → ↓ GFR. Na+/H2O and urea retained by kidney in an attempt to conserve volume → ↑ BUN/creatinine ratio (urea is reabsorbed, creatinine is not) and ↓ FENa.- Urine osmolality >500 mOsm/kg, Urine Na+ <20 mEq/l, FENa <1%, Serum BUN/Cr >20 Intrinsic renal failure: Most commonly due to acute tubular necrosis (from ischemia or toxins); less commonly due to acute glomerulonephritis (eg, RPGN, HUS) or acute interstitial nephritis. In ATN, patchy necrosis → debris obstructing tubule and fluid backflow across necrotic tubule → ↓ GFR. Urine has epithelial/granular casts. Urea reabsorption is impaired → ↓ BUN/creatinine ratio and ↑ FeNa. - Urine osmolality <350 mOsm/kg, Urine Na+ >40 mEq/l, FENa >2%, Serum BUN/Cr <15 Postrenal azotemia: Due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies). Develops only with bilateral obstruction or in a solitary kidney.- Urine osmolality <350 mOsm/kg, rest varies
Consequences of renal failure
Decline in renal filtration can lead to excess retained nitrogenous waste products and electrolyte disturbances. - Na+/H2O retention (HF, pulmonary edema, hypertension)- Hyperkalemia- Metabolic acidosis- Uremia – clinical syndrome marked by ↑ BUN and ↑ creatinine– Nausea and anorexia– Pericarditis– Asterixis– Encephalopathy– Platelet dysfunction- Anemia (failure of EPO production)- Renal osteodystrophy- Dyslipidemia (especially ↑ triglycerides)- Growth retardation and developmental delay
Renal osteodystrophy
Failure of vitamin D hydroxylation, hypocalcemia, and hyperphosphatemia → 2° hyperparathyroidism. - High serum phosphate can bind with Ca2+ → tissue deposits → ↓ serum Ca2+. - ↓ 1,25-(OH)2D3 → ↓ intestinal Ca2+ absorption. - Causes subperiosteal thinning of bones. Clinical features: Weakness, fractures, bone pain, avascular necrosis
Autosomal dominant polycystic kidney disease
Numerous cysts in cortex and medulla causing bilateral enlarged kidneys that ultimately destroy kidney parenchyma. - Presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure in ~50% of individuals. - Mutation in PKD1 (85% of cases, chromosome 16) or PKD2 (15% of cases, chromosome 4). - Death from complications of chronic kidney disease or hypertension (caused by ↑ renin production). - Associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts, diverticulosis. Treatment: If hypertension or proteinuria develops, treat iwth ACE inhibitors or ARBs.
Autosomal recessive polycystic kidney disease
Cystic dilation of collecting ducts. - Often presents in infancy. - Associated with congenital hepatic fibrosis. - Significant oliguric renal failure in utero can lead to Potter sequence. - Concerns beyond neonatal period include systemic hypertension, progressive renal insufficiency, and portal hypertension from congenital hepatic fibrosis.
Autosomal dominant tubulointerstitial kidney disease
Also known as medullary cystic kidney disease.Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine. - Medullary cysts usually not visualized; shrunken kidneys on ultrasound. - Poor prognosis.
Casts in urine
Presence of casts indicates that hematuria/pyuria is of glomerular or renal tubular origin.- Bladder cancer, kidney stones → hematuria, no casts.- Acute cystitis → pyuria, no casts. RBC casts: Glomerulonephritis, hypertensive emergency.WBC casts: Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection.Fatty casts ("oval fat bodies"): Nephrotic syndrome. Associated with "Maltese cross" sign.Granular ("muddy brown") casts: Acute tubular necrosis (ATN).Waxy casts: End-stage renal disease/chronic renal failure.Hyaline casts: Nonspecific, can be a normal finding, often seen in concentrated urine samples.
