CheatSheet: Disorders of Kidney

1. Glomerular Diseases

1.1 Classification

1.2 Minimal Change Disease

• Most common cause of nephrotic syndrome in children (90%)
• Selective proteinuria (albumin only), normal GFR, no hematuria
• Light microscopy: normal glomeruli; EM: podocyte foot process effacement
• Treatment: Corticosteroids - 90% response rate in children
• Associated with Hodgkin lymphoma, NSAIDs

1.3 Focal Segmental Glomerulosclerosis (FSGS)

• Most common primary glomerular disease in adults causing nephrotic syndrome
• Non-selective proteinuria, hematuria, hypertension, progressive renal failure
• Light microscopy: focal and segmental sclerosis; EM: foot process effacement
• Poor response to steroids (20-30%); 50% progress to ESRD in 10 years
• Secondary causes: HIV, heroin, obesity, reflux nephropathy, sickle cell disease

1.4 Membranous Nephropathy

• Most common primary cause of nephrotic syndrome in Caucasian adults
• Anti-PLA2R antibodies in 70% primary cases
• Light microscopy: thickened GBM; IF: granular IgG and C3; EM: subepithelial deposits with spike and dome
• Secondary causes: SLE, hepatitis B, malignancy, NSAIDs, penicillamine
• Rule of thirds: 1/3 remit, 1/3 persistent proteinuria, 1/3 progress to ESRD
• Treatment: ACEi/ARB; immunosuppression if high risk (Cyclophosphamide + steroids or Tacrolimus)

1.5 IgA Nephropathy (Berger Disease)

• Most common primary glomerulonephritis worldwide
• Recurrent gross hematuria within 1-2 days of URTI (synpharyngitic hematuria)
• Mesangial IgA deposition on immunofluorescence
• Henoch-Schonlein Purpura is systemic form with purpura, arthritis, abdominal pain
• Treatment: ACEi/ARB; steroids if proteinuria >1g/day; fish oil
• 25-30% progress to ESRD in 20 years

1.6 Membranoproliferative Glomerulonephritis (MPGN)

• Tram-track appearance on silver stain; mesangial proliferation
• Mixed nephritic-nephrotic presentation

1.7 Post-Infectious Glomerulonephritis

• Follows group A beta-hemolytic Streptococcus infection (pharyngitis/impetigo) by 1-3 weeks
• Acute nephritic syndrome: hematuria, cola-colored urine, hypertension, edema, oliguria
• Low C3, elevated ASO and anti-DNase B titers
• Light microscopy: diffuse proliferative GN; IF: granular IgG and C3 (starry sky); EM: subepithelial humps
• Self-limited in children (>95% recover); worse prognosis in adults
• Treatment: supportive (salt restriction, diuretics, antihypertensives)

1.8 Rapidly Progressive Glomerulonephritis (RPGN)

• Hallmark: crescentic GN on biopsy (>50% glomeruli with crescents)
• Rapid decline in GFR over days to weeks; oliguria, hematuria, RBC casts
• Treatment: pulse methylprednisolone + cyclophosphamide; plasmapheresis for anti-GBM disease

1.9 Alport Syndrome

• X-linked dominant mutation in COL4A5 gene (type IV collagen)
• Hematuria, progressive renal failure, sensorineural deafness, ocular abnormalities (lenticonus)
• EM: GBM splitting (basket-weave appearance)
• Males more severely affected; ESRD by 20-30 years

1.10 Thin Basement Membrane Disease

• Benign familial hematuria; autosomal dominant
• Persistent microscopic hematuria, no proteinuria, normal renal function
• EM: diffusely thin GBM (<250>
• Excellent prognosis; no treatment required

2. Tubular and Interstitial Diseases

2.1 Acute Tubular Necrosis (ATN)

2.2 Acute Interstitial Nephritis (AIN)

• Causes: drugs (beta-lactams, NSAIDs, PPIs, 5-ASA, allopurinol), infections, autoimmune
• Classic triad: fever, rash, eosinophilia (in <10%>
• Urine: eosinophiluria, WBC casts, sterile pyuria, mild proteinuria
• NSAIDs cause AIN with nephrotic-range proteinuria (minimal change disease)
• Biopsy: interstitial inflammation with eosinophils and lymphocytes
• Treatment: stop offending drug, steroids if severe

2.3 Chronic Interstitial Nephritis

2.4 Renal Tubular Acidosis (RTA)

2.5 Fanconi Syndrome

• Generalized PCT dysfunction: aminoaciduria, glycosuria, phosphaturia, bicarbonaturia, uricosuria
• Causes: cystinosis (most common in children), multiple myeloma (adults), ifosfamide, tenofovir
• Rickets/osteomalacia due to phosphate wasting
• Type 2 RTA with hypokalemia

2.6 Bartter and Gitelman Syndromes

• Both: hypokalemic metabolic alkalosis, hyperreninemia, hyperaldosteronism, normal BP

3. Acute Kidney Injury (AKI)

3.1 Definition and Staging (KDIGO)

3.2 Classification

3.3 Prerenal AKI

• Causes: volume depletion (bleeding, GI losses, burns), decreased effective circulating volume (CHF, cirrhosis), renal vasoconstriction (NSAIDs, ACEi/ARBs, HRS)
• Rapidly reversible with volume resuscitation
• If prolonged, progresses to ATN (intrinsic renal failure)

3.4 Intrinsic AKI

• ATN: ischemic or nephrotoxic (see section 2.1)
• Acute interstitial nephritis (see section 2.2)
• Glomerulonephritis: RPGN (see section 1.8)
• Vascular: renal artery thrombosis/stenosis, renal vein thrombosis, atheroembolic disease, TTP/HUS, malignant hypertension

3.5 Postrenal AKI

• Bilateral ureteric obstruction or unilateral in single functioning kidney
• Causes: BPH, prostate cancer, cervical cancer, retroperitoneal fibrosis, bilateral stones, neurogenic bladder
• Diagnosis: ultrasound showing hydronephrosis (may be absent in early obstruction or retroperitoneal fibrosis)
• Treatment: relieve obstruction (catheterization, nephrostomy); watch for post-obstructive diuresis

3.6 Contrast-Induced Nephropathy (CIN)

• Rise in creatinine ≥0.5 mg/dL or ≥25% from baseline within 48-72 hours of contrast
• Risk factors: pre-existing CKD, diabetes, volume depletion, CHF, age >75, contrast volume
• Prevention: IV isotonic saline hydration, minimize contrast volume, hold NSAIDs/diuretics, NAC (controversial)
• Avoid metformin (lactic acidosis risk); restart after 48 hours if renal function stable

3.7 Rhabdomyolysis

• Causes: trauma, prolonged immobilization, seizures, drugs (statins, cocaine), heat stroke, malignant hyperthermia
• Myoglobin causes ATN; serum CK >5000 U/L, hyperkalemia, hyperphosphatemia, hypocalcemia (early), hyperuricemia
• Urine: dipstick positive for blood but no RBCs on microscopy (detects myoglobin)
• Treatment: aggressive IV fluids (200-300 mL/hr), urine alkalinization (sodium bicarbonate), monitor for compartment syndrome

3.8 Tumor Lysis Syndrome

• Massive cell lysis after chemotherapy: hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia
• AKI from uric acid and calcium phosphate precipitation in tubules
• Prevention: allopurinol or rasburicase (preferred if high risk), aggressive hydration, avoid loop diuretics
• Treatment: rasburicase, dialysis if refractory

4. Chronic Kidney Disease (CKD)

4.1 Definition and Staging

• CKD: GFR <60 ml/min/1.73m²="" or="" kidney="" damage="" for="" ≥3="">

4.2 Common Causes

• Diabetes mellitus (40%): most common cause
• Hypertension (25-30%)
• Glomerulonephritis (10-15%)
• Polycystic kidney disease
• Chronic interstitial nephritis

4.3 Clinical Features

4.4 CKD-Mineral Bone Disease

• Decreased phosphate excretion → hyperphosphatemia
• Decreased calcitriol production → hypocalcemia
• Secondary hyperparathyroidism → renal osteodystrophy
• Target PTH: 2-9 times upper limit of normal in ESRD
• Treatment: phosphate binders (calcium carbonate, sevelamer), calcitriol, calcimimetics (cinacalcet)
• Adynamic bone disease: oversuppression of PTH

4.5 Management

4.6 Indications for Dialysis (AEIOU)

• A: Acidosis (refractory metabolic acidosis)
• E: Electrolyte abnormalities (hyperkalemia refractory to medical therapy)
• I: Intoxications (methanol, ethylene glycol, lithium, salicylates)
• O: Fluid overload (refractory to diuretics)
• U: Uremia (pericarditis, encephalopathy, bleeding)
• GFR <15 ml/min="" with="" symptoms="" or="" gfr=""><10>

4.7 Uremic Pericarditis

• Indication for urgent dialysis
• Pericardial friction rub, chest pain, ECG changes
• Risk of hemorrhagic pericardial effusion and tamponade
• Does not respond to NSAIDs (contraindicated in CKD)

5. Cystic Kidney Diseases

5.1 Autosomal Dominant Polycystic Kidney Disease (ADPKD)

• Most common inherited cause of ESRD (10% of ESRD cases)
• PKD1 (85%, chromosome 16, worse prognosis) and PKD2 (15%, chromosome 4)
• Bilateral renal cysts, enlarged kidneys, flank pain, hematuria, hypertension
• Extrarenal: hepatic cysts (most common), cerebral berry aneurysms (5-10%), mitral valve prolapse, colonic diverticula
• Screening: MRI brain for aneurysm if family history of SAH or high-risk occupation
• Treatment: BP control (ACEi/ARB), tolvaptan slows cyst growth and GFR decline
• ESRD by 50-60 years

5.2 Autosomal Recessive Polycystic Kidney Disease (ARPKD)

• PKHD1 gene mutation; presents in infancy/childhood
• Bilateral enlarged cystic kidneys, Potter sequence (oligohydramnios → pulmonary hypoplasia, limb deformities)
• Congenital hepatic fibrosis → portal hypertension, varices, splenomegaly
• Poor prognosis; many die in neonatal period

5.3 Medullary Cystic Kidney Disease

• Autosomal dominant; cysts at corticomedullary junction
• Polyuria, salt wasting, progressive renal failure
• Small kidneys (unlike ADPKD)

5.4 Medullary Sponge Kidney

• Benign condition; dilated collecting ducts in medulla
• Nephrolithiasis (calcium stones), hematuria, UTI, nephrocalcinosis
• Normal renal function; IVP shows contrast-filled cystic spaces (bouquet of flowers)

5.5 Simple Renal Cysts

• Very common; increase with age; no clinical significance
• Bosniak classification for characterizing cysts on CT
• Bosniak I-II: benign; Bosniak IIF: follow-up; Bosniak III-IV: surgical exploration (malignancy risk)

6. Vascular Disorders

6.1 Renal Artery Stenosis (RAS)

• Clinical clues: resistant hypertension, abdominal bruit, flash pulmonary edema, rise in creatinine >30% after ACEi/ARB
• Diagnosis: Doppler ultrasound (screening), CT/MR angiography, gold standard is renal arteriography
• Captopril renography (decreased use now)
• Treatment: ACEi/ARB for medical therapy; angioplasty for FMD (high cure rate); stenting for atherosclerotic (limited benefit)

6.2 Renal Vein Thrombosis

• Causes: nephrotic syndrome (membranous nephropathy, especially), hypercoagulable states, trauma, malignancy
• Acute: flank pain, hematuria, AKI, left testicular swelling (left-sided)
• Chronic: asymptomatic or worsening proteinuria
• Diagnosis: CT/MR venography, Doppler ultrasound
• Treatment: anticoagulation

6.3 Atheroembolic Disease

• Cholesterol emboli to kidneys after vascular procedure or spontaneous in severe atherosclerosis
• Subacute renal failure (days to weeks post-procedure), eosinophilia, eosinophiluria, hypocomplementemia
• Extrarenal: livedo reticularis, blue toe syndrome, GI ischemia, stroke
• Biopsy: cholesterol clefts in arterioles
• No specific treatment; supportive care; poor prognosis

6.4 Renal Infarction

• Causes: atrial fibrillation (embolic), endocarditis, atherosclerosis, trauma, vasculitis
• Sudden flank pain, nausea, fever, hematuria, elevated LDH
• CT with contrast: wedge-shaped perfusion defect
• Treatment: anticoagulation if embolic; thrombolysis if early presentation

6.5 Malignant Hypertension

• BP >180/120 mmHg with acute end-organ damage (retinopathy, AKI, encephalopathy, cardiac)
• Renal: AKI, hematuria, proteinuria, RBC casts
• Biopsy: acute tubular necrosis, fibrinoid necrosis of arterioles
• Treatment: gradual BP reduction over 24-48 hours; IV labetalol, nicardipine, nitroprusside (avoid in renal failure)

6.6 Scleroderma Renal Crisis

• Acute renal failure with malignant hypertension in systemic sclerosis (diffuse cutaneous)
• Microangiopathic hemolytic anemia, thrombocytopenia
• Risk: anti-RNA polymerase III antibodies, early diffuse skin involvement, corticosteroids
• Treatment: ACEi (captopril) started immediately; dialysis if needed (some recover renal function)

7. Thrombotic Microangiopathies

7.1 Hemolytic Uremic Syndrome (HUS)

• Classic triad: microangiopathic hemolytic anemia (schistocytes), thrombocytopenia, AKI
• Normal coagulation profile (PT, aPTT), elevated LDH, low haptoglobin, negative Coombs
• Renal manifestations predominate (unlike TTP)

7.2 Thrombotic Thrombocytopenic Purpura (TTP)

• ADAMTS13 deficiency (cleaves vWF); congenital or acquired (autoantibodies)
• Pentad: microangiopathic hemolytic anemia, thrombocytopenia, AKI, neurologic symptoms, fever
• Neurologic manifestations predominate (headache, confusion, seizures, stroke)
• ADAMTS13 activity <>
• Treatment: plasma exchange (first-line), rituximab, caplacizumab (anti-vWF); avoid platelet transfusion

8. Nephrolithiasis

8.1 Stone Types

8.2 Risk Factors and Causes

8.3 Clinical Presentation

• Acute renal colic: sudden severe flank pain radiating to groin, nausea, vomiting, restlessness
• Hematuria (90% cases), UTI, hydronephrosis, AKI (if bilateral obstruction)
• Diagnosis: non-contrast CT KUB (gold standard); ultrasound in pregnancy

8.4 Management

• Acute: NSAIDs for pain, hydration, medical expulsive therapy (tamsulosin) for stones 5-10 mm
• Indications for intervention: stone >10 mm, obstruction with infection (emergency), intractable pain, AKI
• Procedures: ESWL (stones <20 mm),="" ureteroscopy,="" pcnl="" (large/staghorn="">

8.5 Prevention

9. Diabetic Nephropathy

9.1 Stages

9.2 Pathology

• Kimmelstiel-Wilson nodules: nodular glomerulosclerosis (pathognomonic)
• Diffuse glomerulosclerosis (more common)
• GBM thickening, mesangial expansion, arteriolar hyalinosis
• IF and EM: linear IgG and albumin along GBM

9.3 Clinical Features

• Albuminuria precedes decline in GFR
• Non-nephrotic proteinuria initially, progresses to nephrotic syndrome
• Retinopathy present in >90% cases (if absent, consider other causes)
• Hypertension, accelerated CVD

9.4 Management

• Glycemic control: HbA1c <7%; intensive="" control="" prevents="" onset="" but="" limited="" benefit="" once="">
• BP control: target <130 0;="" acei="" or="" arb="" (first-line,="" antiproteinuric,="">
• SGLT2 inhibitors: reduce albuminuria, slow GFR decline, reduce CV events (canagliflozin, dapagliflozin, empagliflozin)
• GLP-1 agonists: reduce albuminuria and CV events (liraglutide, semaglutide)
• Finerenone (non-steroidal MRA): reduces CKD progression and CV events
• Protein restriction: 0.8 g/kg/day
• Lipid control: statin therapy

10. Hypertensive Nephropathy

10.1 Pathophysiology

• Chronic hypertension → renal arteriosclerosis → ischemic injury → nephrosclerosis
• Benign nephrosclerosis: gradual decline in GFR, mild proteinuria (<1>
• Accelerated by diabetes, smoking, hyperlipidemia

10.2 Pathology

• Arteriolosclerosis: hyaline arteriolosclerosis (benign hypertension), hyperplastic arteriolosclerosis (malignant hypertension)
• Glomerulosclerosis, tubular atrophy, interstitial fibrosis
• Granular contracted kidneys bilaterally

10.3 Clinical Features

• Long-standing hypertension, slowly progressive CKD
• Mild proteinuria, bland urine sediment, no RBC casts
• Left ventricular hypertrophy, retinopathy

10.4 Management

• BP target: <130 0="" mmhg="" in="">
• ACEi/ARB preferred if proteinuria present
• Multi-drug regimen often needed

11. Lupus Nephritis

11.1 ISN/RPS Classification

11.2 Diagnosis

• Renal biopsy required for classification and treatment planning
• IF: full house pattern (IgG, IgA, IgM, C3, C1q); C1q deposition highly specific
• Low C3 and C4 (consume both classical and alternative pathways)
• Anti-dsDNA antibodies correlate with disease activity

11.3 Clinical Features

• Hematuria, proteinuria (nephritic, nephrotic, or mixed), hypertension, renal insufficiency
• Extrarenal lupus manifestations

11.4 Treatment

• Induction (Class III/IV): mycophenolate mofetil or cyclophosphamide + high-dose steroids for 6 months
• Maintenance: mycophenolate or azathioprine + low-dose steroids
• Adjunct: hydroxychloroquine, ACEi/ARB
• Refractory: rituximab, belimumab, voclosporin

12. Renal Transplantation

12.1 Immunosuppression

12.2 Rejection

12.3 BK Virus Nephropathy

• Polyomavirus reactivation in immunosuppressed transplant recipients
• Progressive graft dysfunction; decoy cells in urine
• Diagnosis: BK viremia, viruria; biopsy shows tubular injury with viral inclusions
• Treatment: reduce immunosuppression; cidofovir or leflunomide in severe cases

12.4 Post-Transplant Complications

• Infections: CMV (most common 1-6 months), PCP, Nocardia, Aspergillus, BK virus
• Malignancy: PTLD (EBV-related), skin cancer (SCC > BCC), Kaposi sarcoma
• Recurrent disease: FSGS, IgA nephropathy, membranoproliferative GN, diabetic nephropathy
• New-onset diabetes after transplantation (NODAT): risk with tacrolimus, steroids

13. Acid-Base and Electrolyte Disorders

13.1 Hyperkalemia

• Treatment: calcium gluconate (membrane stabilization), insulin + glucose (shift K into cells), beta-agonists, sodium bicarbonate (if acidotic), loop diuretics, K-binders (patiromer, sodium zirconium cyclosilicate), dialysis

13.2 Hypokalemia

• Causes: GI losses, renal losses (diuretics, RTA, hyperaldosteronism), intracellular shift
• ECG: U waves, flattened T waves, ST depression, prolonged QT
• Complications: muscle weakness, rhabdomyolysis, ileus, arrhythmias
• Treatment: potassium replacement (oral or IV); treat underlying cause

13.3 Hypernatremia

• Hypovolemic: dehydration, GI losses, osmotic diuresis
• Euvolemic: diabetes insipidus (central or nephrogenic), insensible losses
• Hypervolemic: hypertonic saline, hyperaldosteronism
• Treatment: correct slowly (<10-12 meq/l="" per="" 24="" hours)="" to="" avoid="" cerebral="" edema;="" use="" d5w="" or="" hypotonic="">

13.4 Hyponatremia

• Hypovolemic: GI losses, diuretics, renal losses; urine Na <20 (extrarenal)="" or="">20 (renal)
• Euvolemic: SIADH, hypothyroidism, adrenal insufficiency, psychogenic polydipsia
• Hypervolemic: CHF, cirrhosis, nephrotic syndrome; urine Na <>
• Treatment: treat underlying cause; hypertonic saline if severe/symptomatic; fluid restriction in SIADH; tolvaptan (V2 receptor antagonist)
• Correct slowly (<10-12 meq/l="" per="" 24="" hours)="" to="" avoid="" osmotic="" demyelination="">

13.5 Syndrome of Inappropriate ADH (SIADH)

• Euvolemic hypotonic hyponatremia with urine osmolality >100 mOsm/kg and urine Na >40 mEq/L
• Causes: CNS disorders, pulmonary disease (pneumonia, TB), malignancy (SCLC), drugs (SSRIs, carbamazepine, cyclophosphamide)
• Treatment: fluid restriction, salt tablets, demeclocycline, tolvaptan

13.6 Diabetes Insipidus

• Central DI causes: trauma, surgery, tumors (craniopharyngioma), infiltrative (sarcoid, histiocytosis)
• Nephrogenic DI causes: lithium, hypercalcemia, hypokalemia, chronic kidney disease, congenital

13.7 Hypercalcemia

• Causes: hyperparathyroidism (most common outpatient), malignancy (most common inpatient - PTHrP, lytic lesions, calcitriol in lymphoma)
• Other: vitamin D intoxication, granulomatous disease, thiazides, milk-alkali syndrome, immobilization
• Treatment: IV saline, loop diuretics, bisphosphonates, calcitonin, dialysis

13.8 Hypocalcemia

• Causes: hypoparathyroidism, vitamin D deficiency, CKD, hypomagnesemia, acute pancreatitis, tumor lysis
• Clinical: Chvostek sign, Trousseau sign, tetany, seizures, prolonged QT
• Treatment: calcium gluconate (IV if symptomatic), oral calcium, vitamin D; correct hypomagnesemia

14. Urinary Tract Infections and Related Disorders

14.1 Acute Pyelonephritis

• Fever, chills, flank pain, costovertebral angle tenderness, nausea, vomiting
• Urine: pyuria, WBC casts, bacteriuria, positive culture
• Organisms: E. coli (80%), Klebsiella, Proteus, Enterococcus
• Treatment: fluoroquinolone or ceftriaxone for 7-14 days; hospitalize if septic or unable to tolerate oral

14.2 Chronic Pyelonephritis

• Recurrent kidney infections → chronic tubulointerstitial inflammation and scarring
• Causes: VUR, obstruction, chronic stones
• Imaging: cortical scarring overlying blunted calyces
• Treatment: treat UTI, correct anatomic abnormalities

14.3 Xanthogranulomatous Pyelonephritis

• Chronic severe infection with foamy lipid-laden macrophages
• Associated with Proteus infection and staghorn calculi
• CT: enlarged kidney with mass-like appearance
• Treatment: nephrectomy

14.4 Renal Papillary Necrosis

• Ischemic necrosis of renal papillae
• Causes (POSTCARDS): Pyelonephritis, Obstruction, Sickle cell, TB, Cirrhosis, Analgesics (NSAIDs), Renal vein thrombosis, Diabetes, Systemic vasculitis
• Hematuria, flank pain, passing of tissue fragments in urine
• IVP: ring sign or contrast in necrotic papillae

14.5 Perinephric Abscess

• Collection of pus in perinephric space
• Causes: extension from pyelonephritis, hematogenous spread (S. aureus)
• Fever, flank pain persisting despite antibiotics
• CT: fluid collection with rim enhancement
• Treatment: drainage + antibiotics

15. Renal Neoplasms

15.1 Renal Cell Carcinoma

• Risk factors: smoking, obesity, hypertension, VHL, acquired cystic kidney disease in dialysis patients
• Classic triad (10%): hematuria, flank pain, palpable mass
• Paraneoplastic: polycythemia (EPO), hypercalcemia (PTHrP), hypertension (renin), Stauffer syndrome (reversible hepatic dysfunction)
• Metastases: lung, bone, brain; cannonball metastases in lungs
• Diagnosis: CT/MRI abdomen; renal mass protocol CT
• Treatment: partial or radical nephrectomy; sunitinib, pazopanib (VEGF inhibitors), nivolumab (immunotherapy) for metastatic

15.2 Wilms Tumor (Nephroblastoma)

• Most common renal malignancy in children (peak age 2-5 years)
• WAGR syndrome: Wilms, Aniridia, Genitourinary abnormalities, mental Retardation; WT1 gene deletion
• Denys-Drash syndrome: male pseudohermaphroditism, glomerulopathy, Wilms tumor
• Beckwith-Wiedemann syndrome: macroglossia, organomegaly, hemihypertrophy, Wilms tumor
• Presentation: asymptomatic abdominal mass, hematuria, hypertension
• Treatment: nephrectomy + chemotherapy (vincristine, actinomycin D, doxorubicin); excellent prognosis (>90% cure)

15.3 Angiomyolipoma

• Benign tumor composed of blood vessels, smooth muscle, and fat
• Associated with tuberous sclerosis (bilateral, multiple); sporadic cases (unilateral, single)
• Risk of spontaneous hemorrhage if >4 cm
• Diagnosis: CT showing fat density (negative Hounsfield units)
• Treatment: observation if <4 cm;="" embolization="" or="" resection="" if="">4 cm or symptomatic

15.4 Oncocytoma

• Benign renal tumor; mahogany brown with central scar
• Cannot distinguish from RCC on imaging; diagnosed after nephrectomy
• No malignant potential

15.5 Transitional Cell Carcinoma (Urothelial Carcinoma)

• Arises from renal pelvis, ureter, bladder
• Risk factors: smoking, analgesic nephropathy, Balkan nephropathy, cyclophosphamide, aromatic amines
• Painless gross hematuria
• Treatment: nephroureterectomy for upper tract; TURBT for bladder