Vancomycin-Associated Acute Kidney Injury with a Steep Rise in Serum Creatinine.

BACKGROUND: Vancomycin-associated (VA) acute kidney injury (AKI) is being increasingly recognized. A distinct pattern of rapid rise in serum creatinine (sCr) during VA-AKI has occasionally been observed. However, such scenarios remain underreported. METHODS: We conducted an online survey at the American Society of Nephrology Communities forum and reviewed publications of VA-AKI via PubMed or Google searching for cases of precipitous AKI (those with rise in sCr ≥1.5 mg/dL/day) attributable to vancomycin. RESULTS: We identified 12 original cases compiled from 6 different hospitals and 4 published cases (n = 16; 38% women, age 43.5 ± 16 years, weight 108 ± 23 kg, body mass index 35 ± 7 kg/m2) of precipitous AKI observed shortly after large cumulative doses of VA (8.8 ± 5 g). The median steepest 24-h rise in sCr was 2.6 mg/dL (range 1.5-3.5 mg/dL) and the slope of the initial 48-h sCr rise was greater than that of a control AKI (non-VA, n = 48) group (2.03 ± 0.1 vs. 0.62 ± 0.0 mg/dL/day; p < 0.0001). The steep rise in sCr in the VA-AKI was not accompanied by anuria. Overt rhabdomyolysis was absent in all cases. Further, in 3 precipitous VA-AKI cases, simultaneous serum cystatin C values did not rise precipitously, suggesting that the reductions in glomerular filtration rate were overestimated by the sCr increase. CONCLUSIONS: VA-AKI can manifest with a precipitous rise in sCr shortly after a high cumulative dose of vancomycin. True toxic tubular injury overrepresented by the sCr rise is postulated.

Study of various clinical and laboratory parameters among 178 patients affected by hooch tragedy in Ahmedabad, Gujarat (India): A single center experience.

INTRODUCTION/PURPOSE: The outbreak of methanol poisoning described in this paper occurred in Ahmedabad, Gujarat, India in July 2009. Our intention is to share the experience of clinical features, laboratory investigations and their relation during this tragedy. MATERIALS AND METHODS: Single center, retrospective study of clinical features and laboratory parameters of 178 cases of methanol toxicity treated at tertiary care hospital in Ahmedabad, Gujarat. RESULTS: Maximum patients (39.8%, n = 45) were received in 48 h; Mean age of presentation was 41.9 ± 10.2 years. Most of them were men (175 out of 178). On presentation, 83% patients had gastro-intestinal symptoms, 46% had neurological symptoms, 73% had visual symptoms and 32% had dyspnoea. 62% had blurred vision, 10.5% had blindness. Patients with visual symptoms had high mean level of methanol (120.12 ± 23.12 vs. 55.43 ± 29.24, P = 0.014). On fundus examination 52.8% (n = 62) had bilateral hyperaemia of discs, 8.4% (n = 12) had bilateral disc pallor and 4.5% had papilledema (n = 5). Patients with hyperaemia of discs, discs pallor or papilledema, had higher mean methanol level (121.1 ± 32.2 mg% v/s 70.1 ± 23.2 mg%, P = 0.032). Mean of pH values was 7.17 ± 0.22 and bicarbonate was 12.3 ± 7.3 mmol/L. Both pH and bicarbonate levels correlated well with mortality and serum methanol level. Mean serum methanol level was 87.1 mg/dL, and correlated significantly with the mortality (53.1 ± 41 mg/dL v/s 121 ± 92 mg/dL, P value < 0.05). CONCLUSION: GI symptoms, neurological symptoms and breathlessness are important clue to ED physician for diagnose methanol poisoning. Visual symptoms and fundus findings correlate well with the methanol level. Arterial Blood Gas derived pH and bicarbonate levels correlate significantly with the methanol level and mortality.

C1q nephropathy in a child with a chromosome 13 deletion.

C1q nephropathy (C1qNP) is a rare cause of childhood nephrotic syndrome (NS). We describe a child with retinoblastoma, lipomyelomeningocele and a chromosome 13 deletion who presented with massive proteinuria due to C1qNP. Despite steroid resistance, successful treatment of the NS was achieved with mycophenolate mofetil.