Urinary Diagnostic Indices in Acute Renal Failure

Miller, Thomas R.; Anderson, Robert J.; Linas, Stuart L.; Henrich, William L.; Berns, Arnold S.; Gabow, Patricia A.; Schrier, Robert W.

doi:10.7326/0003-4819-89-1-47

Cited by 404 publications

(139 citation statements)

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“…This is particularly true for acute glomerulonephritis, acute interstitial nephritis, and pyelonephritis. Moreover, although urine sediment analysis is considered a part of the clinical workup of kidney disease in hospitalized patients with AKI, its true value in improving diagnosis is not clearly known (1)(2)(3)(4)(5). Furthermore, there has been a gradual trend away from using the simple, inexpensive, and rapid modality of urine microscopy in the evaluation of AKI.…”

Section: Discussionmentioning

confidence: 99%

“…The diagnosis of AKI is currently and primarily based on measurement of serum creatinine, blood urea nitrogen, and urine output. In addition to these parameters, urine biochemistry and microscopy provide the vital information in the differentiation of AKI into traditional categories of prerenal azotemia and acute tubular necrosis (ATN) (1)(2)(3)(4)(5). Therapies and prognosis for prerenal AKI and ATN differ substantially; therefore, early clinical differentiation is important.…”

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confidence: 99%

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Diagnostic Value of Urine Microscopy for Differential Diagnosis of Acute Kidney Injury in Hospitalized Patients

Perazella

Coca

Kanbay

et al. 2008

Clinical Journal of the American Society of Nephrology

160

132

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Background and objectives: Urine microscopy is the oldest and one of the most commonly used tests for differential diagnosis of acute kidney injury (AKI), but its performance has not been adequately studied in the setting of AKI.Design, setting, participants, & measurements: Fresh urine samples were obtained from 267 consecutive patients with AKI, and urinary sediment was examined. The cause of AKI was assessed at two time points: (1) Before urine microscopy diagnosis and (2) after patient discharge or death (final diagnosis). A urinary scoring system also was created on the basis of casts and renal tubular epithelial cells (RTEC) to differentiate acute tubular necrosis (ATN) from prerenal AKI.Results: The urinary sediment scoring system was highly predictive of the final diagnosis of ATN. In patients with a high pretest probability of ATN (initial diagnosis of ATN), any casts or RTEC (score >2) resulted in very high positive predictive value and low negative predictive value for a final diagnosis of ATN. In patients with a low pretest probability of ATN (initial diagnosis of prerenal AKI), lack of casts or RTEC on urinary sediment examination had a sensitivity of 0.73 and specificity of 0.75 for a final diagnosis of prerenal AKI. The negative predictive value of lack of casts or RTEC in patients with low pretest probability of disease was 91%.Conclusions: Urine sediment examination is a valuable diagnostic tool for confirming the diagnosis of ATN. A score of >2 on an ATN urinary sediment scoring system is an extremely strong predictor of ATN.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Diagnostic Value of Urine Microscopy for Differential Diagnosis of Acute Kidney Injury in Hospitalized Patients

Perazella

Coca

Kanbay

et al. 2008

Clinical Journal of the American Society of Nephrology

160

132

View full text Add to dashboard Cite

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“…23 The TAL plays an important role in the kidney's capacity to concentrate urine because Na reabsorbed in the TAL is critical for maintaining the countercurrent exchange mechanism by generating a hypertonic medullary interstitium; therefore, loss of Na-K-2Cl co-transport in the TAL abolishes the medullary concentration gradient, resulting in an inability to concentrate urine even in the presence of vasopressin. Our GCV-injured transgenic mice exhibited defects in urinary con-centration not corrected by the vasopressin analogue DDAVP, suggesting that these mice have lost their medullary concentration gradient secondary to failure of TAL Na transport.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis of the Thick Ascending Limb Results in Acute Kidney Injury

Srichai¹,

Hao²,

Davis³

et al. 2008

Journal of the American Society of Nephrology

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Ischemia-or toxin-induced acute kidney injury is generally thought to affect the cells of the proximal tubule, but it has been difficult to define the involvement of other tubular segments because of the widespread damage caused by ischemia/reperfusion or toxin-induced injury in experimental models. For evaluation of whether thick ascending limb (TAL)-specific epithelial injury results in acute kidney injury, a novel transgenic mouse model that expresses the herpes simplex virus 1 thymidine kinase gene under the direction of the TAL-specific Tamm-Horsfall protein promoter was generated. After administration of gancyclovir, these mice demonstrated apoptosis only in TAL cells, with little evidence of neutrophil infiltration. Compared with control mice, blood urea nitrogen and creatinine levels were at least five-fold higher in the transgenic mice, which also developed oliguria and impaired urinary concentrating ability. These findings suggest that acute injury targeted only to the TAL is sufficient to cause severe acute kidney injury in mice with features similar to those observed in humans. 19: 153819: -154619: , 200819: . doi: 10.1681 Acute kidney injury (AKI), which contributes significantly to morbidity and mortality among hospitalized patients, 1 is frequently multifactorial, 2 with ischemia and nephrotoxins being the most common causes. Regardless of cause, histologic findings include dilated and flattened epithelium, loss of tubular epithelial cells, and the presence of TammHorsfall protein (THP)-rich casts. Frank necrosis is not usually apparent, and apoptotic cells are consistently found in both ischemic and nephrotoxic forms of clinical AKI. 3,4 At the cellular level, actin cytoskeletal abnormalities lead to loss of cell polarity and relocation of cell adhesion molecules. 5,6 Endothelial dysfunction and inflammation are present, although morphologic changes are subtle. 7,8 A key unanswered question in AKI is how the kidney protects itself from devastating losses of body fluids as a result of the failure of glomerular ultrafiltrate reabsorption. One proposed mechanism is tubuloglomerular feedback (TGF), whereby increased distal delivery of solutes to the macula densa results in feedback signals to the glomerulus to decrease GFR by afferent arteriole constriction. After injury, tubular epithelial cell reabsorption of sodium is impaired, which results in increased distal delivery of NaCl and subsequent activation of TGF. The decreased renal blood flow and GFR result in oliguria and, in severe cases, anuria. This J Am Soc Nephrol

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“…In the setting of impaired renal perfusion, low urine sodium concentration and fractional excretion of sodium, elevated urine osmolality, and elevated urine-plasma creatinine ratio indicate preserved tubular function and an appropriate renal response to the prerenal azotemic state. With the onset of ATN, tubular dysfunction leads to an increase in urinary sodium concentration and fractional excretion of sodium ([urine sodium/plasma sodium]/[urine creatinine/plasma creatinine] ϫ 100), and an impairment in urinary concentrating capacity characterized by a decrease in urine osmolality and urine-plasma creatinine ratio (9). The physician must be aware, however, that advanced chronic renal failure and recent diuretic use may alter the utility of these urinary measures.…”

Section: Diagnosis Of Atnmentioning

confidence: 99%