Urinary Final - Acute And Chronic Renal Failure

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Def: AKI

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Rapid loss (over hours - sev days) of nephron function, resulting in azotemia and/or fluid, electrolyte, and acid-base abnormalities

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Four stages of AKI

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Initiation phase
Extension phase
Maintenance phase
Recovery phase

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Initiation phase

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during and immeidately following insult to kidneys, when pathologic damage to kidneys is initiated

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Extension phase

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ischemia, hypoxia, inflammation, ance cellular injury continue, leading ot cell apoptosis and/or necrosis

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Maintenance phase

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may be the first stage to see clin/lab abnormalities. characterized by azotemia and/or uremia. Lasts for days to weeks. Oliguria (10 ml per pound per day) or anuria (<2 ml per pound per day) may occur.

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Recovery

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azotemia improves and renal tubules undergo repair. Polyurea may occur during this stage as the result of partial restoration of renal tubular function and of osmotic diuresis of accumulated solutes.

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Most common causes of AKI

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nephrotoxicity, infection, and ischemia

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Acute glomerular disease

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Rare, but horses can develop membranoproliferative glomerulonephritis secondary to equine infectious anemia or strangles.

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Role of Gastrin in uremia

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Hormone that stimulates parietal cells of the gastric mucosa to secrete acid. Increased gastrin may casuse gastric inflammation and ulceration.

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Role of PTH in uremia

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Seconday hyperparathyroidism in chronic renal failure results in removal of calcium from bone.

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Nephrotoxins that cause Ischemia

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1.) NSAIDs: inhibiting prostacyclin in the rena medulla, can cause medullary and papillary ischemia. May also induce inflammatory interstitial reaction.
2.) Cisplatin: renal vasoconstriction leading to ischemic injury in the tubules. May be directly toxic to tubules.

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Nephrotoxins that cause increased membrane permeability

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Amphotericin B: forms pores on the tubular plasma membrane increasing membrane permeability

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Nephrotoxins that cause intratubular crystal formation

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1.) Melamine/cyanuric acid
2.) Hyperuricosuria: dalmatians have faulty uric acid transport (liver and kidney) from the catabolism of purines leading to excess uric acid in renal tubules.
3.) Cysteinuria: tubular cells can't reabsorb cysteine leading to cysteine crystals.
4.) Ethylene glycol. metabolized to glycolic acid and causes metabolic acidosis. Further metabolized to oxalic acid, which precipitates.

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Aminoglycoside nephrotoxicity

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Freely filtered into glomerulus and taken up by tubular cells where it induces lysosomal damage.

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Mycotoxins: fumonisin B nephrotoxicity

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Interferes with sphingolipids in tubular cells and causes cell death somehow

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Hemoglobin and myoglobin nephrotoxicity

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Iron can be directly toxic to tubular epithelial cells via ROS production. Myoglobin can also cause vasoconstriciton leading to ischemia.

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Heavy metal nephrotoxicity

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Metal salts more toxic since they're more water soluble. Bind to sulfahydryl groups on proteins and inhibit cell functions

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Fanconi syndrome (acquired or inherited)

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Tubules fail to reabsorb glucose, AA, Na, PO4, and HCO3-. Basenji most commonly affected. Acquied forms due to copper toxicity.

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Urolith def'n

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Organized, polycrystalline concretion found in the urnary tract and containing primarily organic or inorganic crystalloids and a much smaller amount of organic matrix

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Calculus def'n

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Genearl term referring to a solid concretion formed in ducts or hollow organs