Diseases in Nephrology (AKI and CKD) Flashcards
Associated with multiple myeloma
Renal amyloidosis
MOST common form of AKI
Prerenal azotemia
MOST common cause of CKD
DM
Patchy necrosis, PCT and LH affected, relatively short length of tubules affected
Ischemic type ATN (e.g. in hypovolemia)
Extensive necrosis, PCT and DT affected, relatively longer lengths of tubules affected
Toxic type ATN (e.g. in use of aminoglycosides, radio-contrast dyes)
Acts as an essential mediator of increased intraglomerular capillary pressure by selectively increasing efferent arteriolar vasoconstriction relative to afferent arteriolar tone
Angiotensin II
MAJOR pathway for reducing excess total body K+
Renal excretion
THREE broad categories of AKI
Prerenal azotemia
Intrinsic renal disease
Postrenal obstruction
MOST common clinical conditions associated with prerenal azotemia
Hypovolemia
Decreased cardiac output
Medications that interfere with renal autoregulatory responses such as NSAIDs and inhibitors of angiotensin II
MOST common causes of intrinsic AKI
Sepsis
Ischemia
Nephrotoxins
Usual clinical course of contrast induced nephropathy
A rise in SCr beginning 24-48 hours following exposure
Peaking within 3-5 days
Resolving within 1 week
MOST common protein in urine and produced in the thick ascending limb of the loop of Henle
Uromodulin/Tamm-Horsfall Protein
Large kidneys observed in patients with CKD suggest the following:
Diabetic nephropathy
HIV-associated nephropathy
Infiltrative diseases
Occasionally acute interstitial nephritis
Provide DEFINITIVE diagnostic and prognostic information about AKIs and CKDs
Kidney biopsy
Hallmark of AKI
Buildup of nitrogenous waste products, manifested as an elevated BUN concentration (azotemia)
Definitive treatment of the hepatorenal syndrome
Liver transplantation
Continuous Renal Replacement Therapy is often PREFERRED in patients with
Severe hemodynamic instability
Cerebral edema
Significant volume overload