Acute tubular necrosis and pre-renal acute kidney injury: utility of urine microscopy in their evaluation- a systematic review

A man with a history of alcoholism presented on two different occasions with mental changes, clinical signs of volume depletion, elevated serum osmolal gap, metabolic acidosis with high anion gap, metabolic alkalosis, hyponatremia, and azotemia after binge drinking of only ethanol. In both episodes, the serum contained ethanol, acetone, and 2-propanol (isopropanol), but no methanol or ethylene glycol. In the first episode, the rates of excretion of acetoacetate and 3-hydroxybutyrate in the urine were greatly increased. Volume repletion was the only treatment. In both episodes, azotemia and metabolic acidosis were rapidly reversed, while modest metabolic alkalosis was noted after treatment. The triad of azotemia, elevated osmolal gap, and high anion gap metabolic acidosis, which characterizes intoxication with methanol or ethylene glycol, can also develop in alcoholic ketoacidosis (AKA), an entity with substantially different management and outcome. Finding 2-propanol in the serum of patients with AKA indicates either concomitant 2-propanol ingestion or formation of 2-propanol from acetone.

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“…Urine microscopy [8] revealed few dark brown granular casts, but no crystals. Urine sodium concentration was 9 mmol/l.…”

Section: First Episodementioning

confidence: 97%

Repeated intoxication presenting with azotemia, elevated serum osmolal gap, and metabolic acidosis with high anion gap: differential diagnosis, management, and prognosis

et al. 2010

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“…These urine biochemical tests have traditionally been used as a method to categorize AKI into states of “pre-renal azotemia”, whereby AKI may be milder and reversible (UNa <20 mmol/L; FeNa < 1%; FeU <35%), and “acute tubular necrosis” (ATN), whereby AKI is more severe and established (UNa >40 mmol/L; FeNa >2%; FeU >35%). In addition, no studies have utilized novel biomarkers of kidney “damage” such as neutrophil gelatinase-associated lipocalin (NGAL) to evaluate the diagnostic and prognostic value of urine biochemistry in AKI [12]. …”

Section: Introductionmentioning

confidence: 99%

Urine biochemistry in septic and non-septic acute kidney injury: a prospective observational study

Bagshaw¹,

Bennett²,

Devarajan³

et al. 2013

Journal of Critical Care

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Purpose Determine whether there are unique patterns to the urine biochemistry profile in septic compared with non-septic acute kidney injury (AKI) and whether urinary biochemistry predicts worsening AKI, need for renal replacement therapy and mortality. Materials and Methods Prospective cohort study of critically ill patients with septic and non-septic AKI, defined by the RIFLE (Risk, Injury, Failure, Loss, End-Stage) criteria. Urine biochemistry parameters were compared between septic and non-septic AKI and were correlated with neutrophil gelatinase-associated lipocalin (NGAL), worsening AKI, renal replacement therapy (RRT), and mortality. Results Eighty-three patients were enrolled, 43 (51.8%) with sepsis. RIFLE class was not different between groups (P = .43). Urine sodium (UNa) <20 mmol/L, fractional excretion of sodium (FeNa) <1%, and fractional excretion of urea (FeU) < 35% were observed in 25.3%, 57.8%, and 33.7%, respectively. Septic AKI had lower UNa compared with non-septic AKI (P = .04). There were no differences in FeNa or FeU between groups. Urine NGAL was higher for FeNa≥1% compared to FeNa<1% (177.4 ng/mL [31.9-956.5] vs 48.0 ng/mL [21.1-232.4], P = .04). FeNa showed low correlation with urine NGAL (P = .05) and plasma NGAL (P = .14). There was poor correlation between FeU and urine NGAL (P = .70) or plasma NGAL (P = .41). UNa, FeNa, and FeU showed poor discrimination for worsening AKI, RRT and mortality. Conclusion Urine biochemical profiles do not discriminate septic and non-septic AKI. UNa, FeNa, and FeU do not reliably predict biomarker release, worsening AKI, RRT or mortality. These data imply limited utility for these measures in clinical practice in critically ill patients with AKI.

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“…1 The prevalence of AKI in all hospitalized patients is 5-35%, which is associated with a two-to five-fold increased mortality risk. 2 Neutrophil gelatinase-associated lipocalin (NGAL, also known as Lipocalin 2) has been shown to be dramatically induced early in ischemic renal injury (IRI) by use of cDNA microarrays. 3 The small 25kDa peptide is a secret protein, initially found in human neutrophils 4,5 with its mouse analog 24p3 belonging to the lipocalin superfamily.…”

Section: Introductionmentioning

confidence: 99%

Neutrophil Gelatinase-Associated Lipocalin (NGAL) May Play a Protective Role Against Rats Ischemia/Reperfusion Renal Injury via Inhibiting Tubular Epithelial Cell Apoptosis

Zang

Wang

et al. 2012

Renal Failure

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We investigated the protective effect and mechanism of neutrophil gelatinase-associated lipocalin (NGAL) on rats ischemia/reperfusion (I/R) renal injury. Eighteen Sprague-Dawley male rats were randomly divided into three groups. Control group (n ¼ 6) suffered left unilateral nephrectomy, I/R þ NS (normal saline) (n ¼ 6) and I/R þ NGAL (n ¼ 6) group were subjected to 45 min right renal ischemia/24 h reperfusion after left unilateral nephrectomy. Serum creatinine (Scr) and blood urea nitrogen (Bun) were measured on automatic biochemistry analyzer; kidney sections were stained with hematoxylin-eosin; terminal dUTP nick-labeling method was used to examine the apoptosis of tubular epithelial cells; Cleaved caspase-3 and Bax protein expression were detected by immunohistochemistry and Western Blot; real-time polymerase chain reaction was used to detect the expression of Bax mRNA. Rats with NGAL displayed an attenuated renal damage and a decreased number of tubular epithelial cell apoptosis compared to the I/R þ NS group (Scr 63.400 AE 11.908 vs. 121.857 AE 17.151 μmol/L, Bun 14.840 AE 2.868 vs. 28.557 AE 6.434 mmol/L, apoptosis cell number 7.800 AE 1.924 vs. 15.400 AE 3.049/high power field (HPF), p < 0.05), the values were lower in the control group (24.000 AE 3.829 μmol/L, 5.814 AE 1.961 mmol/L, 1.800 AE 0.837/HPF, p < 0.05) compared to two groups above; NGALtreated rats showed down-regulated Cleaved caspase-3 protein (0.284 AE 0.066 vs. 0.409 AE 0.073, p < 0.05), Bax protein (0.346 AE 0.055 vs. 0.443 AE 0.041, p < 0.05), Bax mRNA (1.423 AE 0.187 vs. 2.550 AE 0.217, p < 0.05) compared to I/R þ NS group, but the values were higher in both of the two groups than those in the control group (Cleaved caspase-3 protein 0.104 AE 0.029, Bax protein 0.155 AE 0.027, Bax mRNA 1.000 AE 0.000, p < 0.05). We supposed that exogenous NGAL can inhibit the activation of caspase-3, reduce the expression of Bax, and thus reduce renal tubular cell apoptosis and protect renal function in I/R injury rats.

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Acute tubular necrosis and pre-renal acute kidney injury: utility of urine microscopy in their evaluation- a systematic review

Cited by 46 publications

References 39 publications

Repeated intoxication presenting with azotemia, elevated serum osmolal gap, and metabolic acidosis with high anion gap: differential diagnosis, management, and prognosis

Repeated intoxication presenting with azotemia, elevated serum osmolal gap, and metabolic acidosis with high anion gap: differential diagnosis, management, and prognosis

Urine biochemistry in septic and non-septic acute kidney injury: a prospective observational study

Neutrophil Gelatinase-Associated Lipocalin (NGAL) May Play a Protective Role Against Rats Ischemia/Reperfusion Renal Injury via Inhibiting Tubular Epithelial Cell Apoptosis

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