RSL - Renal Flashcards
Extracellular compartments:
70kg
- 60% water (42L)
- 1/3 extracellular fluid (14L)
- 75% interstitial fluid (10.5L)
- 25% plasma (3.5L)
- 2/3 intracellular fluid (28L)
- 10% RBC volume (2.8L)
- 1/3 extracellular fluid (14L)
- 40% non-water mass (28kg)
Fanconi Syndrome
(and causes)
Causes: PCT
- Hereditary defects:
- Wilson’s disease,
- tyrosinemia,
- glycogen storage disease,
- Ischemia
- Multiple myeloma
- Nephrotoxins: Expired tetracyclines, tenofovir,
- Lead poisoning
Bartter
Thick ascending loop of henle: Na/K/2Cl
- Hypokalemia
- metabolic acidosis
- Hypercalciuria
Gitelman syndrome
DCT
- Hypokalemia
- Hypomagnesemia
- Metabolic alkalosis
- Hypocalciuria
Liddle syndrome
Collecting duct: gain of function (ENaC)
- Hypokalemia
- metabolic alkalosis
- decreased aldosterone
Treat: amiloride
Syndrome of apparent mineralocorticoid excess
Collecting duct: (11 B-hydroxysteroid dehydrogenase)
- Hypokalemia,
- hypertension
- metabolic alkalosis
Can be acquired from glycyrrhetic acid
Na+ Low/High serum conc.
Low:Nausea, malaise, stupor, coma, seizures
High: Irritability, stupor, coma
K+ low/high []
[Ca++] low/high
Low Ca++: tetany, seizures, GT prolongation
High Ca++: Kidney stones, Bone pain, diahrea, increased urinary freq, psychiatric changes
[Mg++] low/high
Low: Tetany, torsades de pointes, hypokalemia
High: Decreased DTRs, Lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
[PO4—]
Low: Bone loss, osteomalacia, rickets
High: Renal stones, metastatic calcifications, hypocalcemia
Distal (type 1), urine pH >5.5
Defect in alpha intercalated cells
- –> no H+ secretion
- –> no HCO3- regeneration –> Acidosis
- –> Kidney stones
- –> no H+/K+ exchange –> hyperkalemia
- –> no HCO3- regeneration –> Acidosis
Causes:
- Amphotericin B, analgesic nephropathy, congenital anomalies of urinary tract
Proximal (type 2), Urine pH <5.5
PCT HCO3- reabsorption:
- increased HCO3- excretion –> metabolic acidosis
- Na+ not reabsorbed –> increased Acid/K+ loss
- Hypokalemia, low pH
Causes: fanconi syndrome, CA inhibitors
Hyperkalemic (type 4), urine pH <5.5
Hypoaldosteronism
- hyperkalemia –> decreased NH3 synthesis in PCT –> decreased NH4+ excretion
Causes:
- Low aldosterone (diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDS, heparin, cyclosporine, adrenal insufficiency
- Aldosterone resistance (K+ sparing diuretics, nephropathy due to obstruction, TMP/SMX)
Post streptococcal Glomerulonephritis
(LM/IF/EM)
LM: Hypercellular glomeruli that is enlarged
IF: Starry sky granular appearance. Lumpy bumpy due to IgG, IgM, C3 deposition in GBM and mesangium
EM: Subepithelial imunne complex humps
Rapidly progressive Glomerulonephritis
(LM/IF)
LM/IF: Crescent moon shape consisting of fibrina and plasma proteins with glomerular parietal cells, monocytes, macrophages
Good pasture syndrome
Type II hypersensitivity –> ab to GBM and Alveolar basement membrane –> hematuria/hemoptysis
Granulomatosis with polyangitis (wegener)
PR3-ANCA / c-ANCA
(sinusitis; not seen in good pastures)
Microscopic polyangitis
MPO-ANCA / p-ANCA
Diffuse proliferative glomerulonephritis
(LM/IF/EM)
(DT/)
LM: wire looping of capillaries
IF: granular
EM: subendothelial and sumetimes intramembranous IgG based IC often with C3 deposition
Often nephrotic / nephritic concurrently
Dt/ SLE or membranoproliferative glomerulonephritis
IgA nephropathy (Berger disease)
(LM/IF/EM)
(disease)
LM: Mesangial proliferation
IF: IgA based IC deposits in mesangium
EM: mesangial IC deposits
DT/ Henoch-Schönlein purpura
Alport syndrome
(mutation)
(symptoms)
(EM)
Type IV collagen mutation –> thinning and splitting of GBM
Symp: Eyes, glomerulonephritis, sensorineural deafness
EM: Basket weave appearance
Membranoproliferative glomerulonephritis
Type 1: (EM/IF/PAS)(association)
Type 2: (EM)
1: hep B / C
- EM: Subendothelial immune complex deposits
- IF: granular
- PAS (LM): tram track appearance
2: C3 nephritic factor (stabolizes C3 convertase)
* EM: intramembranous IC deposits; dense deposits
Focal segmental glomerulosclerosis
(LM/IF/EM)
(Associations)
Treat:
LM: Segmental sclerosis and hyalinosis
IF: Non-specific deposits of IgM, C3, C1
EM: Effacement of foot processes similar to minimal change disease
Associations: African american, Hispanic, HIV, Sickle cell, Obesity, Heroin use, IFN treatment,
Treat: inconsistent response to steroids