Renal Flashcards
Where does horseshoe kidney get stuck?
IMA
Where is horseshoe kidney adjoined?
Lower Poles
Potter Syndrome
- lung hypoplasia
- flat face with low set ears
- Limb defects
All due to oligohydraminos from bilateral renal agenesis
How to DDx Dysplastic Kidney disease from PKD
Dysplastic Kidney Disease is NOT inherited and can be uni or bilateral
PKD is always bilateral
Autosomal Recessive PKD presentation
BILATERAL enlarged kidneys w/ cysts in medulla/Cx
Presents in infants with renal failure and HTN
May have Potter Syndrome
ARPKD associated with
Congenital hepatic fibrosis and hepatic cysts
Autosomal dominant PKD presentation
young adult with HTN (high renin), hematuria, worsening renal failure
ADPKD associations
Berry anneurysms, hepatic cysts, MVP
Think cysts in vessels, heart, and liver
ADPKD genetic mutations
APKD1 & APKD2 gens
Medullary Cystic Kidney Disease
Cysts in medullary collecting ducts
parenchymal fibrosis leads to SHRUNKEN kidney and worsening renal failure
Acute renal failure hallmarks
Azotemia (increased BUN and Creatinine) often with oliguria
Prerenal Azotemia
Decreased blood flow to kidney
leads to decreased GFR, azotemia, and oliguria
Prerenal azotemia labs
BUN:Creatinine > 15 (normal 15)
FENa < 1%
Urine Osmolarity > 500 mOsm/kg
Kidney is still functioning so some BUN is reabsorbed
Postrenal Azotemia
Urinary Tract obstruction increases back pressure decreasing GFR
Also forces BUN back into blood
azotemia and oliguria
Early Postrenal azotemia Labs
BUN:Creatinine > 15
FENa < 1%
Urine Osmo > 500
looks just like prerenal azotemai
Late postrenal azotemia labs
BUN:creatinine < 15
FENa > 2%
Urine Osmo < 500
Acute Tubular Necrosis
Injury/necrosis of tubular epithelial cells
Plug tubules decreasing GFR
Brown Casks in urine
Acute Tubular Necrosis Labs
BUN:Creatinine < 15
FENa > 2%
Urine Osmo <500
Etiology of Acute tubular necrosis
Ischemia, Nephrotoxic (Rx, heavy metals, urate, etc.)
Clinical features of Acute tubular necrosis
oliguria with brown casts
elevated BUN and Creatinine
Hyperkalemia
Metabolic Acidosis (increased anion gap)
Tx acute tubular necrosis
dialysis, remove toxin
2-3 week recovery
tubular cells are stable cells so they take time to reenter cell cycle
Acute Interstitial Nephritis
Rx induced hypersensitivity involving interstitium and tubules
NSAIDs, penicillin, diuretics
Acute Interstitial Nephritis Sx
Fever, oliguria, rash days to weeks after start of Rx
Eosinophils in urine
Acute Interstitial nephritis Tx
Stop Rx
Renal Papillary Necrosis
Necrosis of renal papillaries
Gross hematuia and flank pain
Renal Papillary Necrosis Causes
DM, analgesic abuse, Sickle cell, acute pyelonephritis
Minimal Change Disease associated with
hodgkins lymphoma
1 Nephrotic Syndrome in kids
Minimal Change Disease
Histo of Minimal Change disease
Effacement of foot processes which leads to selective proteinuria (only albumin)
Glomerulus pretty much looks normal
Tx or Minimal Change Disease
Steroids
Due to pathogenesis: Cytokines mediate damage
Nephrotic Syndromes associated with HBV and HCV
Focal Segmental Glomerulonephritis
Type I membranoproliferative glomerulonephritis
Nephrotic syndromes with foot process effacement
Minimal change disease
Focal Segmental glomerulosclerosis
Focal segmental glomerulosclerosis findings
Some glomeruli (focal)
involving only part of glomerulus (segmental)
sclerosis
effacement of foot processes
Spike and Dome appearance
Grainy Immunofluorescence
Membranous Nephropathy
Complex deposition is subepithelial
No response to steroids
Nephrotic Syndromes with negative immunofluorescence
Focal segmental glomerulosclerosis
Minimal change disease
Who gets Focal Segmental Glomerulosclerosis? Associations?
Hispanics and Af. Am.
Sickle Cell, Heroin, HIV
Most common nephrotic syndrome in Caucasian adults
Membranous Nephropathy
Membranous Nephropathy associations
Whites
HBV/HCV
SLE
Rx (NSAIDs, Penicillamine)
Subendothelial complex deposition
Tram track appearance
HBV/HCV associated
Membranoproliferative disease type I
Intramembranous complex deposition
Associated with C3 nephrotic factor
unregulated complement
Membranoproliferative Type II
C3 nephrotic factor stablizes C3 convertase –> complement does not get shut off
Membranoproliferative histo
Thick glomerular basement membrane due to complex deposition
poor response to steroids
Think of thickening (proliferation) of the basement membrane (membranous)
DM Nephrotic findings
HYALINE ARTERIOLOSCLEROSIS
High serum glucose leads to nonenzymatic glycosylation of vascular basement membrane
Tx of DM nephrotic Sx
ACE
Hyaline deposits in efferent arteriole. ACE prevents Angiotensin II vasocontriction of efferent arteriole decreasing Sx
Kimmelstiel Wilson Nodules
Diabetes Mellitis
sclerosis of mesangium
Apple Green apple birefringenc after Congo Red stain
Deposits in mesangium
Systemic Amyloidosis
Kidney is most common organ involved
Why are nephritic syndromes hypercellular?
Immune complexes deposit activating complement.
C5a attracts neutrophils mediating damage to kidney