Renal Flashcards
Fanconi syndrome: causes
Hereditary (Wilson's dz, glycogen storage dz) Multiple myeloma Ischemia Lead tox Drugs (expired tetracyclines, tenofovir)
Renal tubular defects
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Fanconi Bartter Gitelman Liddle (Loud = gain of fxn) SAME
Things excreted and by where in Fanconi syndrome
PCT defect
Don’t reabsorb: amino acids, glucose, HCO3, PO4
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Acute interstitial nephritis:
Classic findings
P’s
Less common causes
Pyuria: EOSINOPHILS - no casts Pee (diuretics) Pain-free (NSAID's, Chronic ASA+Aceto) PCN (and ceph) PPI rifamPin
Systemic infection, autoimmune (Sjogren, SLE, sarcoid)
Actue tubular necrosis causes
Ischemic (decreased renal blood flow)
Nephrotoxic (AG, contrast, crush injury)
Muddy brown casts
Renal papillary necrosis
SAAD papa
SCD
Acute pyelonephritis
Analgesics
Diabetes mellitus
Crescent formation pathophys
Macs and T cells pass into Bowman’s space
Fibrin leaks in via gaps in the membrane
Macs secrete factors than enhance deposition
Fibroblasts infiltrate and secrete collagen
Potter’s sequence:
Usual cause
Usual finding
Usually a renal cause that leads to decreased urinary output
Flat face, lower limb deformity, pulmonary hypoplasia, renal agenesis
Renal plasma flow =
PAH clearance
(urine PAH x flow rate) / plasma PAH
Renal blood flow =
PAH clearance / 1-hematocrit
Ammonia buffer system:
Stimulus
Starting amino acid
End result
Acidosis stimulates
Glutamine is broken down in tubule cell
Ammonia secreted into lumen and bicarb into blood
Do you replace catheters?
Nope! So stop picking that answer
Type of incontinence in MS
Urge incontinence
Spastic bladder
Spastic bladder vs. flaccid bladder
Spastic: hypertonia, frequency throughout day
Flaccid: increased residual volume, incontinence towards end of day
Transplant rejection path findings
Hyperacute (minutes/hours): preformed antibodies; cyanosis, arterial fibrinoid necrosis/thrombosis
Acute (<6mo): humoral (C4d depletion, neuts, nec vasculitis); cell mediated (lymphs)
Chronic (months-years): low grade immune response (suppresants); wall thickening, lumen narrowing, interstitial fibrosis, atrophy
You finally learned what the allantois is?
Three abnormalities, go:
Allantois = urachus in urogenital sinus Remnant can lead to: 1. patent -> umbilical discharge 2. urachal sinus (failure to close distal) -> infection 3. cyst (middle persists)
Repeat positive RPR assay -> next steps?
TP-EIA assay looking for trep. pal.
If neg -> SLE, especially anti-phospholipid-antibodies (prolonged PTT)
Worst prognostic factor for PSGN?
Adult onset -> less likely to fully recover
Where is the macula densa?
How about the JG cells?
Who secretes renin?
Macula densa -> distal tubule (sense hypoperfusion and stimulate JG cells)
JG cells -> in afferent arteriole (secrete renin)
ADH upregulates what in the kidney?
TWO THINGS!
- Aquaporins in CT
- Urea in the medullary collecting duct
Consequences of renal failure
MAD HUNGER Met Acidosis Dyslipidemia (inc. trigly) Hyperkalemia Uremia Na+ retention Growth retardation/developmental delay EPO failure Renal osteodystrophy (dec. vit D, inc. PTH, low Ca2+)
Side effects of EPO therapy
Indicated with GFR<30
Thromboembolic events
HTN (via EPO receptors on vascular smooth muscle)
Causes of anion ion gap metabolic acidosis
MUDPILES
Methanol Uremia DKA Propolene glycol INH, Infection Lactic acidosis Ethylene glycol Saliycates
Clear cell renal carcinoma histo findings
Big, clear cells
Glycogen and lipid accumulation in cells
IgG4 and anti-phospholipase A2
1˚ membranous nephropathy
Dietary risk for kidney stones
Low fluid Low calcium High oxalate High protein High sodium High fructose
Disease risk factors for kidney stones
1˚ hyperparathyroidism: high Ca
Cronhs: hyperoxaluria
Distal RTA: low citrate
Gout: high uric acid
High citrate in the urine prevents sontes
Serum and urine findings (most commonly) with kidney stone
Hypercalciuria
Normocalcemia
Most and least concentrated parts of a nephron
Most: bottom of loop
Least: top of PCT
Aldosterone effects on CT and Na, K, HCO3 findings in primary aldosteronism
Na+ in (which negatively charges lumen)
Pulls K+ and H+ out -> met alk, hypoK
However, Na remains normal in 1˚ aldo
Na: nml
K+: low
HCO3: high
