Pathoma: Kidney & Urinary Tract Pathology Flashcards
Horseshoe Kidney
Congenital Disorders
Conjoined kidneys usually connected at lower poles & abnormally located in lower abdomen
- Horseshoe kidney gets caught on root of IMA during ascent from pelvis to abdomen
Most common congenital renal anomaly
Horseshoe Kidney
Renal Agenesis
Congenital Disorders
Absence of kidney formation
* May be unilateral or bilateral
* Unilateral–> hypertrophy of existing kidney
* Compensatory hyperfiltration
* Increases sirk of renal failure later in life
* Bilateral –> oligohydramnios; Potter sequence
* Lung hypoplasia
* Flat face low set eats
* Limb abnormalities
* Incompatible with life
Dysplastic Kidney
Congenital Disorders
Spontaneous congenital malformation of renal parenchyma characterized by cysts & abnormal tissue
* Usually unilateral; when bilateral, must be distinguished from polycystic kidney disease
Polycystic Kidney Disease (PKD)
Congenital Disorders
Inherited defect leading to bilateral kidney enlargement with cysts in renal cortex & medulla
* Autosomal recessive PKD: presents in infants
* Worsening renal failure & HTN
* Neonates may present w/ Potter sequence
* Associated w/ congenital hepatic fibrosis (leads to portal HTN) & hepatic cysts
* Autosomal dominant PKD: presents in adults
* HTN, hematuria, & worsening renal failure
* Cysts develop over time due to mutation in APKD1 or APKD2 gene
* Associated w/ berry aneurysm, hepatic cysts, & mitral valve prolapse
Medullary Cystic Kidney Disease (MCKD)
Autosomal dominant defect leading to cysts in medullary collecting duct
* Parenchymal fibrosis results in shrunken kidneys & worsening renal failure
Acute Renal Failure (ARF)
General
Acute, severe decrease in renal function
* Develops within days
* Hallmark: azotemia (increased BUN & Cr)
* Often with oliguria
* Divided into prerenal, postrenal, and intrarenal based on etiology
Prerenal Azotemia
Decreased renal perfusion
* Results in decreased GFR, azotemia, & oliguria
* Reabsorption of fluid & BUN
* Serum BUN:Cr > 15
* Tubular function remains intact
* FENa < 1%
* uOsm > 500
Postrenal Azotemia
Outflow obstruction downstream of kidney
* Back pressure decreases GFR, azotemia, & oliguria
* Early stage: increased tubular pressure drives fluid & BUN into blood
* Serum BUN:Cr > 15
* Tubular function remains intact
* FENa < 1%
* uOsm > 500
* Late stage: increased pressure damages tubule, impairing reabsorption of fluid & BUN
* Serum BUN:Cr ratio < 15
* Decreased Na+ reabsorption (FENa > 2%)
* Inability to concentrate urine (uOsm < 500)
Acute Tubular Necrosis (ATN)
Intrarenal Azotemia
Injury & necrosis of tubular epithelial cells
* Necrotic cells shed & plug tubules
* Obstruction back pressure decreases GFR
* Brown, granular casts seen in urnie
* Dysfunctional tubular epithelium:
* Decreased BUN reabsorption
* Serum BUN:Cr ratio < 15
* Decreased Na+ reabsorption
* FENa > 2%
* Inability to concentrate urine
* Urine osm < 500 mOsm/kg
ATN
Etiology
- Ischemia: decreased perfusion results in ATN
* Often preceded by prerenal azotemia
* PCT & medullary TAL are particularly susceptible to ischemic damage - Nephrotoxicity: toxic agents result in ATN
* Proximal tubule is particularly susceptible
* Causes: aminoglycosides, heavy metals, myoglobinuria., ethylene glycol, radiocontrast dye, uric acid
- Oliguria with brown, granular casts
- Elevated BUN & Cr
- Hyperkalemic metabolic acidosis
Presentation
ATN
Acute Interstitial Nephritis
Intrarenal Azotemia
Drug-induced HSR involving interstitium & tubules resulting in ARF
* Causes: NSAIDs, penicillin, diuretics
- Oliguria, fever, & rash days to weeks after starting a drug
- Hallmark: urine eosinophilia
Presentation
Acute Interstitial Nephritis
Renal Papillary Necrosis
ARF
Necrosis of renal papillae
* Presents with gross hematuria & flank pain
* Causes: chronic analgesic abuse; DM; sickle cell disease; severe acute pyelonephritis
