Anuria/Oliguria Case Closing- Ratliff- 2/1/2013
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| 2 most common causes of chronic kidney disease that predispose to development of acute kidney injury in setting of other exposures | Diabetes and hypertension
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| "I am not making much urine" goes under which section of a note | Chief complaint
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| By which mechanism does an ACE inhibitor increase risk of AKI | It blocks the conversion of Angiotensin I to Angiotensin II which inhibits vasoconstriction of the efferent arteriole which is needed to maintain GFR in decreased blood pressure or volume
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| Effect of NSAID on Renal Blood flow | Vasoconstricts afferent arteriole
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| Effect of ANP on Renal Blood flow | Vasodilates afferent arteriole
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| Effect of Prostaglandin on Renal Blood flow | Vasodilates afferent arteriole and vasoconstricts efferent arteriole
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| Effect of Angiotensin II on Renal Blood flow | Vasoconstricts efferent arteriole
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| Effect of Norepinephrine on Renal Blood flow | Vasoconstricts efferent arteriole
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| Effect of ACE inhibitor on Renal Blood flow | Vasodilates efferent arteriole
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| Rash in a kidney patient can be indicative of | Glomerulonephritis or autoimmune (lupis)
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| Frothy urine is indicative of | Proteinuria
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| Tea colored urine is indicative of | Hematuria or rhabdomylosis
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| Tachycardia, hypotension, reduced skin turgor with tenting and syncope are all findings supporting | Volume depletion
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| Definitive way of diagnosing post-renal causes | Ultrasound
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| Increased Lactic acid levels are due to | Ischemia/hypoperfusion
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| Lack of blood and protein in the urine points to | Pre-renal causes
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| In pre-renal disease, a decreased flow leads to increased reabsorption of | BUN
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| A BUN:CR for pre-renal etiologies | >20
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| Decreased pressure and flow lead to activation of | RAAS
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| Urine sodium levels for pre-renal etiologies | <20
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| Explain why urine sodium levels are low in pre-renal disease | In cases of depleted volume, Kidneys will activate RAAS and maximally reabsorb sodium and therefor increasing water retention. This will happen as long as TUBULES ARE INTACT
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| RBCs or RBC casts are indicative of | Intrinsic glomerular disease
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| "Muddy brown" granular casts are indicative of | Intrinsic Tubular disease
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| WBCs and WBC casts with a negative urine culture are indicative of | Intrinsic Interstitial disease
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| High BUN:CR and Low Na+ points to | Pre-renal disease
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| Low BUN:CR and high Na+ points to | Intrinsic renal disease
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| High BUN:Cr and high Na+ points to | Post-renal disease
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| Pre-renal etiology is due to | True volume depletion or medications affecting renal blood flow
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| Plan for patient with pre-renal causes | IV fluid hydration and holding potential offending medications
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| Anuria | Absence of urine formation (<100 ml/day)
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| Oliguria | Scanty urine production (<400-500 ml/day)
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| Normal urine production | >500 ml/day
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| Nephrotoxic | Toxic to renal cells
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| Nephritic | Relating to or suffering from nephritis
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| Nephritis | Inflammation of the kidneys (RBC in urine)
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| Nephrotic | Relating to, caused by, or similar to nephrosis
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| Nephrosis | Damage to renal tubular epithelium/glomerular basement membrane (protein in urine)
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| General cause of prerenal disease | Less fluid is delivered to the kidneys for filtration
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| General cause of intrinsic renal disease | The kidneys are unable to produce urine to due intrinsic disease
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| General cause of Postrenal disease | The kidneys are obstructed and urine cannot be excreted
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| Nephritic urine sediment suggests | Glomerulonephritis
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| Sterile pyuria suggests | Interstitial nephritis
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| Proteinunuria suggests | Intrinsic/Glomerular process
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