scholarly journals Acute kidney injury with partial Fanconi syndrome in a patient with leptospirosis: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Marc Weiner ◽  
Matteo Coen ◽  
Jacques Serratrice ◽  
Thomas A. Mavrakanas ◽  
Antonio Leidi
Keyword(s):  
Acute Kidney Injury ◽  
Case Report ◽  
Kidney Injury ◽  
Liver Function Tests ◽  
Immunoglobulin M ◽  
Lower Limbs ◽  
Tubular Dysfunction ◽  
Kidney Dysfunction ◽  
Diagnostic Challenge ◽  
Amoxicillin Clavulanate

Abstract Background Leptospirosis is an underdiagnosed bacterial infection with nonspecific symptoms, hence, a diagnostic challenge. Identifying a case of leptospirosis in Switzerland is uncommon. Although kidney complications are frequent in severe forms, including tubular dysfunction, observing this complication is rare in our country. We report the case of a patient with leptospirosis and kidney dysfunction, which was notable for proximal tubulopathy. This case report describes the diagnosis and management of this patient’s tubular dysfunction. Case presentation A 34-year-old Caucasian male known for alcohol and drug abuse presented to our emergency department suffering from severe pain in the lower limbs, jaundice, and fever with flu-like symptoms. Physical examination was not contributory. Blood tests showed cytopenia, elevated inflammatory markers, acute kidney injury, and altered liver function tests with predominant cholestasis. Urinalysis showed proteinuria and significant glycosuria without concomitant hyperglycemia. Leptospirosis was suspected and confirmed by both positive serum polymerase chain reaction and elevated immunoglobulin M for Leptospira interrogans. The patient was treated with intravenous amoxicillin–clavulanate and doxycycline for 7 days. After antibiotic treatment, symptoms disappeared, and kidney dysfunction completely resolved. Conclusion Our case focuses on the description of leptospirosis-related acute kidney injury with proximal tubular dysfunction, which is a rare finding in Switzerland.

scholarly journals Proteomic Characterization of Acute Kidney Injury in Patients Hospitalized with SARS-CoV2 Infection

2021 ◽  
Author(s):  
Ishan Paranjpe ◽  
Pushkala Jayaraman ◽  
Chen-Yang Su ◽  
Sirui Zhou ◽  
Steven Chen ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Myocardial Damage ◽  
Hemodynamic Instability ◽  
Tubular Dysfunction ◽  
Kidney Dysfunction ◽  
Post Discharge ◽  
Longitudinal Measurements ◽  
Increased Risk

AbstractAcute kidney injury (AKI) is a known complication of COVID-19 and is associated with an increased risk of in-hospital mortality. Unbiased proteomics using longitudinally collected biological specimens can lead to improved risk stratification and discover pathophysiological mechanisms. Using longitudinal measurements of ∼4000 plasma proteins in two cohorts of patients hospitalized with COVID-19, we discovered and validated markers of COVID-associated AKI (stage 2 or 3) and long-term kidney dysfunction. In the discovery cohort (N= 437), we identified 413 upregulated and 40 downregulated proteins associated with COVID-AKI (adjusted p <0.05). Of these, 62 proteins were validated in an external cohort (p <0.05, N =261). We demonstrate that COVID-AKI is associated with increased markers of tubular injury (NGAL) and myocardial injury. Using estimated glomerular filtration (eGFR) measurements taken after discharge, we also find that 25 of the 62 AKI-associated proteins are significantly associated with decreased post-discharge eGFR (adjusted p <0.05). Proteins most strongly associated with decreased post-discharge eGFR included desmocollin-2, trefoil factor 3, transmembrane emp24 domain-containing protein 10, and cystatin-C indicating tubular dysfunction and injury. Using longitudinal clinical and proteomic data, our results suggest that while both acute and long-term COVID-associated kidney dysfunction are associated with markers of tubular dysfunction, AKI is driven by a largely multifactorial process involving hemodynamic instability and myocardial damage.

Serial Quantification of Urinary Protein Biomarkers to Predict Drug-induced Acute Kidney Injury

2019 ◽  
Vol 20 (8) ◽  
pp. 656-664 ◽  
Author(s):  
Yi Da ◽  
K. Akalya ◽  
Tanusya Murali ◽  
Anantharaman Vathsala ◽  
Chuen-Seng Tan ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cystatin C ◽  
Calcineurin Inhibitors ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Protein Biomarkers ◽  
Drug Induced ◽  
Beta 2 ◽  
Beta 2 Microglobulin

Background: : Drug-induced Acute Kidney Injury (AKI) develops in 10-15% of patients who receive nephrotoxic medications. Urinary biomarkers of renal tubular dysfunction may detect nephrotoxicity early and predict AKI. Methods:: We prospectively studied patients who received aminoglycosides, vancomycin, amphotericin, or calcineurin inhibitors, and collected their serial urine while on therapy. Patients who developed drug-induced AKI (fulfilling KDIGO criteria) were matched with non-AKI controls in a 1:2 ratio. Their urine samples were batch-analyzed at time-intervals leading up to AKI onset; the latter benchmarked against the final day of nephrotoxic therapy in non- AKI controls. Biomarkers examined include clusterin, beta-2-microglobulin, KIM1, MCP1, cystatin-C, trefoil-factor- 3, NGAL, interleukin-18, GST-Pi, calbindin, and osteopontin; biomarkers were normalized with corresponding urine creatinine. Results:: Nine of 84 (11%) patients developed drug-induced AKI. Biomarkers from 7 AKI cases with pre-AKI samples were compared with those from 14 non-AKI controls. Corresponding mean ages were 55(±17) and 52(±16) years; baseline eGFR were 99(±21) and 101(±24) mL/min/1.73m2 (all p=NS). Most biomarker levels peaked before the onset of AKI. Median levels of 5 biomarkers were significantly higher in AKI cases than controls at 1-3 days before AKI onset (all µg/mmol): clusterin [58(8-411) versus 7(3-17)], beta-2-microglobulin [1632(913-3823) versus 253(61-791)], KIM1 [0.16(0.13-0.76) versus 0.07(0.05-0.15)], MCP1 [0.40(0.16-1.90) versus 0.07(0.04-0.17)], and cystatin-C [33(27-2990) versus 11(7-19)], all p<0.05; their AUROC for AKI prediction were >0.80 (confidence intervals >0.50), with average accuracy highest for clusterin (86%), followed by beta-2-microglobulin, cystatin-C, MCP1, and KIM1 (57%) after cross-validation. Conclusion: : Serial surveillance of these biomarkers could improve the lead time for nephrotoxicity detection by days.

Successful treatment of decompression sickness complicated with acute hepatic infarction and acute kidney injury: a case report

2019 ◽  
pp. 81-85
Author(s):  
Se Hyun Oh ◽  
◽  
Hui Dong Kang ◽  
Sang Ku Jung ◽  
Sangchun Choi ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Case Report ◽  
Hyperbaric Oxygen ◽  
Successful Treatment ◽  
Decompression Sickness ◽  
Kidney Injury ◽  
Pressure Change ◽  
Hepatic Infarction ◽  
Hbo2 Therapy

Decompression sickness is a disease caused by abrupt pressure change and presents various symptoms. To date, acute kidney injury associated with decompression sickness has been reported frequently, but there is no report of hepatic infarction associated with decompression sickness. We report a case of acute kidney injury and acute hepatic infarction treated with hyperbaric oxygen (HBO2) therapy and dialysis in a patient with severe decompression sickness after work diving.

Rhabdomyolysis, Acute Kidney Injury, and a Novel Frameshift Mutation in a Child with Glutaric Acidemia Type I

Nephron ◽  
2021 ◽  
pp. 1-6
Author(s):  
Linlin Huang ◽  
Ting Shi ◽  
Ying Li ◽  
Xiaozhong Li
Keyword(s):  
Acute Kidney Injury ◽  
Case Report ◽  
Frameshift Mutation ◽  
Novel Mutation ◽  
Kidney Injury ◽  
Febrile Illness ◽  
Type I ◽  
Continuous Venovenous Hemodiafiltration ◽  
Glutaric Acidemia Type I ◽  
Acute Decompensation

This is a case report of a girl with glutaric acidemia type I (GA-I) who experienced rhabdomyolysis and acute kidney injury (AKI). Her first acute metabolic crisis occurred at the age of 5 months, which mainly manifested as irritable crying, poor appetite, and hyperlactatemia. Mutation analysis showed 2 pathogenic mutations in the glutaryl-CoA dehydrogenase (GCDH) gene, which were c.383G&#x3e;A (p.R128Q) and c.873delC (p.N291Kfs*41), the latter of which is a novel frameshift mutation of GA-I. She had a febrile illness at the age of 12 months, followed by AKI and severe rhabdomyolysis. Four days of continuous venovenous hemodiafiltration (CVVHDF) helped to overcome this acute decompensation. This case report describes a novel mutation in the GCDH gene, that is, c.873delC (p.N291Kfs*41). Also, it highlights the fact that patients with GA-I have a high risk of rhabdomyolysis and AKI, which may be induced by febrile diseases and hyperosmotic dehydration; CVVHDF can help to overcome this acute decompensation.

scholarly journals The Use of Supra-Hemodiafiltration in Traumatic Rhabdomyolysis and Acute Kidney Injury: A Case Report

2021 ◽  
pp. 26-35
Author(s):  
Gabriele Donati ◽  
Maria Cappuccilli ◽  
Federica Di Filippo ◽  
Simone Nicoletti ◽  
Marco Ruggeri ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Case Report ◽  
Septic Patient ◽  
Medical Therapy ◽  
Kidney Injury ◽  
First Case ◽  
Successful Recovery

Oliguric acute kidney injury due to traumatic rhabdomyolysis can be potentially lethal if the proper medical therapy combined with extracorporeal detoxification is not performed. Different extracorporeal techniques are available to overcome this syndrome. Here, we report the first case of removal of myoglobin and successful recovery from acute kidney injury in an elderly septic patient using supra-hemodiafiltration with endogenous reinfusion technique (HFR-Supra) combined with the medical therapy.

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