Renal System Flashcards
Acute Kidney Injury
(Pre-Renal)
Caused by decr renal perfusion;
BUN/creatinine ratio typically >20:1
Fractional excreti Na+ <1%
Urine osmolality >500 mOsm/kg
Microscopy Hyaline casts
Acute Kidney Injury
(Post-Renal)
Caused by urinary tract obstruction with normal nephron capacity. Etiologies include bilateral calculi, enlarged prostate, or a renal tumor in an individual with a sole functional kidney.
Bilateral Hydronephrosis is also seen.
Acute Kidney Injury
(Intra Renal)
Aka Acute Tubular Necrosis
Renal ischemia (eg, hemorrhage, sepsis) or nephrotoxins (eg, aminoglycosides, radiocontrast)
Can also present in setting of cardiac ischemia due likely episode of Hypotension.
BUN/Cr Typically ~10-15
Fractional excretion Na+ >2%
Urine Osm ~300 mOsm/kg
Microscopy Muddy brown casts
PSGN
(Post Streptococcal Glomerluonephritis)
Aka Proliferative glomerulonephritis/ Acute glomerulonephritis
After streptococcal inf i.e Strep Pyogenes (2 wks) can present as 1-3 wks of red urine after sore throat.
Periorbital Edema
Hypertension
Micro/Gross Hematuria
Type-3 Hypersenstivity reaction (Antigen-Antibody complex that form in blood and deposit in kidney)
child recovers well, poor prognosis in adults
LM: hypercellular enlarged glomeruli.
IF: Granular deposits of IgG, IgM, C3 on GBM & Mesangium (lumpy-bumpy).
EM: Subepithelial humps b/w podocytes and GBM
Increase Anti-streptolysin-O & Anti-DNase B-titers
Decrease complement protien C3
Fanconi syndrome
Polyuria, renal tubular acidosis type II, growth retardation, electrolyte imbalances, hypophosphatemic rickets
(multiple combined dysfunction of the PCT)
Impaired PCT reabsorbtion of AA, Glucose, PO4–, HCO3–.
Caused by consumption of expired Tetracyclines.
HUS (Hemolytic-uremic syndrome)
In children, Predominately caused by Shiga toxin–producing Escherichia coli (STEC) infection (serotype O157:H7)
- Thrombocytopenia
- Hemolytic Anemia
- Acute kidney Injury
- Bloody Diarrhea
ADPKD
( Autosomal dominant polycystic kidney disease )
Genetic mutation in polycystin ( PKD1 , PKD2 )
Multiple large cysts in kidneys due to structural abnormalities in renal tubules.
Inherited with complete penetrance & Variable expressivity.
Can present with:
Flank pain, Hematuria, HTN, Progressive CKD.
PSGN
most common in kids;
sub epithelial humps - IgG, C3, and C4 deposition;
lumpy bumpy on EM;
ASO antibodies
Membranous Proliferative Glomerulonephritis
tram-tracks on LM, basement splitting
Urge Incontinence
urgency leads to complete voiding,
detrusor spasticity leads to small bladder volume;
PVRV: 5-10mL
RTA Type-2
Inability of PCT to reabsorb bi-carb (HCO3–).
proximal RTA = bad carbonic anhydrase, lost all bicarb in urine
Focal Segmental Glomerulonephritis
Seen in
IV drug abusers, African Americans, Hispanics, and HIV patients
Overflow Incontinence
cannot completely empty bladder
PVRV: residual volume > 100ml
Minimal Change Disease
Most common nephrotic syndrome in kids
fused foot processes on EM, no renal failure, loss of charge barrier
Membranous Glomerulonephritis
Most common nephrotic syndrome in adults
LM: BM spikes,
EM: sub epithelial spikes and domes
IF: granular/ linear
Stress Incontinence
weak pelvic floor muscles
urinating when coughing, laughing, etc.
estrogen effect;
PVRV = 50ml
RTA Type-1
Inability of DCT to secrete Proton (H+).
distal (DCT) RTA = H+/K+ exchange in collecting duct is broken,
high urine pH (low H+ in urine)
Barter Syndrome
@ ascending loop
JG cell hyperplasia with renin excess;
no increase in blood pressure;
defect in kidney’s ability to reabsorb potassium
–presents like chronic loop diuretic use–
SIADH
( Syndrome of Inappropriate Anti-Diuretic Harmone )
Too much ADH (Vasopressin)
ADH is produced by supraoptic nucleus of hypothalamus and stored in posterior pituitary.
ADH increases water reabsorption in medullary collecting duct.
↓Serum Osmolality , ↓Serum specific gravity
↓ serum Na (< 135)
↑ Urine osmolality , ↑ Serum specific gravity
Tx :
– Demeclocycline (tetracycline causes insenstivity to ADH).
– Conivaptan & Tolvaptan (ADH receptor antagonists).
