Renal 3 Flashcards
What are the associated conditions for renal papillary necrosis?
> Sickle cell disease/trait: sickled cells obstruct kidney vessels, predisposing to ischemia.
Analgesic nephropathy: NSAIDs inhibit renal blood flow.
DM: metabolic abnormalities cause changes in vascular wall (nonenzymatic glycosylation).
Pyelonephritis: edematous interstitium compresses medullary vasculature, ischemia
What is the pentad of ssx for TTP-HUS? (FRANTic condition)
Fever Renal failure Anemia Neuro sx (progressive lethargy) Thrombocytopenia *In the setting of GI illness
Thrombotic microangiopathy (TMA) syndromes all have what 4 features?
> Platelet activation in arterioles and capillaries
Diffuse microvascular thrombosis (brain, kidney, heart)
Hemolytic anemia w/ schistocytes
Thrombocytopenia
Thiazide diuretics
[MOA, SE]
Decrease BP by dec. blood volume, CO, SVR.
>Inhibits NaCl reabsorption in DCT.
>Dec. blood volume partially attenuated by activated RAAS – inc. aldosterone – inc. K, H excretion – Hypokalemia, metabolic alkalosis.
SE: muscle weakness, cramps
Why are patients with bilateral renal artery stenosis in danger of renal failure when taking ACE inhibitors?
Normally, w/ GFR already decreased due to stenosis, there will be inc. renin and thus inc. AT2, w/c will cause efferent arteriolar constriction, resulting in inc. GFR. However, a patient taking ACEi will block this response, and so GFR is further decreased in bilateral RAS.
What sort of diuretics should be given to congested heart failure patients, and why?
IV loop diuretics block NaCl reabsorption, decreasing the medullary concentration gradient. W/o a hypertonic renal medulla, water has less osmotic driving force to leave the collecting ducts, thus increasing excretion of NaCl and water.
Why would only thiazide diuretics present with hyponatremia and not loop diuretics?
Thiazide diuretics can maintain a normal medullary concentration gradient, so they can better reabsorb water in response to inc. ADH at the collecting ducts – better able to retain free water in relation to Na concentration. Loop diuretics lose both NaCl and water due to lack of hypertonic renal medulla.
How can NSAIDs cause kidney injury?
Chronic NSAID use can cause interstitial nephritis, papillary necrosis, and tubular atrophy. NSAIDs can uncouple oxidative phosphorylation and possibly cause glutathione depletion – damage to tubular and endothelial cells (Renal papillary necrosis, renal interstitial nephritis).
Why is Acetazolamide also useful in patients w/ glaucoma?
Acetazolamide is a diuretic that inhibits carbonic anhydrase, effectively blocking NaHCO3 and water reabsorption in the PCT. Carbonic anhydrase is also found in the eyes where it modulates HCO3 and aqueous humor formation. It can dec. IOP in glaucoma.
How are insulin and normal saline used to treat DKA?
> Insulin: cells use glucose as energy source; dec. lipolysis, dec. ketone bodies – inc. HCO3 since no ketones to bind, intracellular shift of K (beware of hypokalemia, need K repletion).
Normal saline: rehydration, normalize serum Na, dec. serum osmolarity
What is a renal complication of Lithium?
Lithium antagonizes ADH action in the collecting ducts, so it reduces the ability to concentrate urine. This can cause Nephrogenic DI, w/c is resolved w/ discontinuation of lithium.
What are the dietary and disease risk factors for nephrolithiasis?
> Dietary intake: dehydration, low calcium, high sodium, high oxalate, high protein, high fructose.
Diseases: primary hyperparathyroidism (hypercalciuria), Crohn disease (hyperoxaluria), Distal RTA (hypocitraturia), Gout (hyperuricosuria).
What conditions is Minimal change disease commonly associated with, and why?
MCD is caused by immune dysregulation, so it’s associated w/ respiratory infections, immunizations, and atopic d/o.
Immune dysfunction leads to inc. glomerular permeability factor, a cytokine that damages podocytes and decreases anionic properties of GBM (selective albuminuria)
Acute renal failure in children is commonly caused by what syndrome?
Hemolytic uremic syndrome often develops ff. a diarrheal illness caused by a Shiga toxin-producing microbe (EHEC, Shigella). It presents w/ a triad: microangiopathic hemolytic uremia, thrombocytopenia, AKI.
What is a common finding that can identify if someone has ingested ethylene glycol?
Calcium oxalate crystals in the urine are due to metabolism of ethylene glycol, which yields oxalic acid metabolite.
There is also the ballooning and vacuolar degeneration of PCT cells, leading to acute tubular necrosis.
