Path 20: Kidney no make pee Flashcards
Post strep glomerulonephiritis timeline and IF/EM
1-4 weeks
Granular staining pattern for IgG and C3 humps of immune complexes
Renal tubular acidosis types
1: Distal renal
2: Proximal renal
4: Hyperkalemic
Distal renal tubular acidosis pathogenesis
Inability of α-intercalated cells to secrete H+
Distal renal tubular acidosis findings
Decreased serum K+.
Urine pH above 5.5
Renal tubular acidosi: what type of acidosis ?
Normal anion gap
Proximal renal tubular acidosis pathogenesis
PCT HCO3 reabsorption is impaired leading to increased urine HCO3
Hyperkalemic tubular acidosis pathogenesis
Hypoaldosterone or aldosterone resistance leads to hyperK. Leads to decreased NH4 excretion
Labs in type 4 tubular acidosis
Increased serum K+
Fanconi sx sumptoms
Generalized PCT reabsoroption defect. Leads to excretion of all PCT absorbed sunstances
Barter syndrome pathogenesis and findings
Na/+K+/2Cl- defect
Acts like lasix
Metabolic alkalosis, hypoK, hypercalciuria
Liddle syndrome caused by
Gain of function leads to decrease in Na+ degredation and increase in Na+ reabsorption in collecting tubule
RBC casts seen with
Glomerolonephritis, HTN
WBC casts seen in
Tubulointerstitial inflamation, pyelonephritis
Granular casts seen in ? and appearance
Acute tubular necrosis
“Muddy brown”
Fatty casts seen in and visual
Nephrotic syndrome
Maltese cross
Waxy casts seen in
ESRF
Neprhitic syndrome presentation
Hematuria, RBC casts, oligouria, HTN
Nephritic syndrome etiology
Glomerula inflammation leads to GBM damage
Leads to RBC loss and hematuria
Nephrotic syndrome etiology
Podocyte damage fucks with charge barrier leading to proteinuria
Nephrotic syndrome findings
Massive proteinuria with edema, frothy urine, hypercoagulable state
PSGN post strep pathology
2-4 weeks after strep infection. Type III hypersensitivity
PSGN light IF
Starry sky/ granular appearance.
IgG, IgM and C3 deposition in GBM and mesangium
PSGN Electron microscopy
Subepithelilial IC humps
RPGN features
Rapid deterioration, cresents
RPGN and linear IF:
Goodpasture syndrome (Type II hypersensitivity)
RPGN and negative IF:
Granulomatosis
C-ANCA, MPO-ANCA, p-ANCA
RPGN and Granular IF
diffuse proliferative glomerulonephritis
Diffuse proliferative glomerulonephitis seen with
Lupus
Diffuse proliferative glomerulonephritis EM
Sub endothelial deposit
IgA nepropathy aka
Berger dx
Berger disease presentation
IGA vasculitis due to current GI/Resp infection
IgA nepropathy IF
On mesangium, granular
Alport syndrome pathogenesis
Type IV collagen mutation
Glomerular basement membrane loss of integrity
Minimal change disease pathology
Nephrotic syndrome in children
Due to foot process effacement
Focal segemental glomerulosclerosis LM/EM findings
LM: segemental sclerosis and hyalinosis
EM: effacement of foot processes
Membranous nepropathy pathogenesis
Usually idiopathic GBM thickening
Membranous nepropathy LM/IF/EM findings
IF: granular
LM: thick GBM and capillary
EM: spike and dome subepithelial
Amylodisosis finding
Apple green birefringence
Diabetic glomerulonephropathy pathology
Hyperglycemia leads to glycation of proteins
leads to increads GBM membrane. Causes hypterfiltration
Drugs that help diabetic nephropathy
ACE inhibitor
Calcium stone features
Radiopaque , can be calciuria,
Ammonium magnesium phosphate stones aka ____ + features
Struvite
Radiopaque
Caused by infections that hydrolyze urea
Coffin cristal
Elevated urine ph causes precipitation of
Calcium phosphate
Ammonium magnesium phosphate
Hypocitriuria causes precipitation of
Calcium oxalate
Decreased urine ph causes precipitation of
Uric acid
Cystine
Uric acid stone features
Radiolucent
Rhomboid crystal
Seen in diseases with rapid cell turnover
Cystine stone features
Seen in cystinuria, hexagonal crystals
Staghorn caliculi stone types
Infections (struvite)
Cystine
Chronic pyelonephritis pathology
Interstitial fifrosis, usually due to obstruction.
Atrophic tubules lead to thyrodization
Prerenal azotemia due to
Hypovolemia
Prerenal azotemia BUN/CR
More than 20
Postrenal azotemia BUN:Cr
less than 15
Acute interstitial nephritis pathology
Drug induced hypersensitivity to NSAIDs, PCN and diuretics
Acute interstitial nephritis presentation
Oliguria, fever, rash. No pain.
Pyuria, azotemia
Acute tubular necrosis presentation
Acute renal failure, hyperK, metabolic acidosis, uremia, increased FENA+, unconcentrated urine
Renal papillary necrosis presentation
Gross hematuria and flank pain, often inciting event
Renal failure consequences
Metabolic acidosis
HyperK
Sodium retention
Autosomal dominant kidney disease presentation and gene
Cysts where
APKD1/2 gene mutation. Presents as young adult with HTN and renal failure
Cyts in medulla and cortex
autosomal dominant PKD treatment
ACE inhibitors
ARBs
Autosomal recessive PKD features
Potter seuqnece, congenital hepatic fibrosis, cysts in collecting ducts .
Renal cell carcinoma presentation
Hematuria, papable mass, flank pain
Fever, weight loss, paraneoplastic syndrome
Renal cell carcinoma gene progression
Loss of VHL gene (chromosome 3)
Most common malignant renal tumor in kids
Wilms tumor (avg 3yo)
Wilms tumor pahtology
Malignant tumor made of blastema (mesenchyme)
Wilms tumor presentation
Palapable mass, hematuria, HTN
Wilms tumor with no iris and malformed genitals
WAGR complex
wilms tumor with WT1 deletion
WAGR
Wilms tumor with hypoglycemia, hypertrophy of tongue and muscles (+gene)
Beckwith-Wiedman
WT2
Membranous nepropathy caused by (virus)
HepB