scholarly journals Acute kidney injury, metabolic acidosis, and hypercalcemia with proximal tubular dysfunction—a diagnostic challenge: Questions

2021 ◽  
Author(s):  
Adem Yasin Köksoy
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Diagnostic Challenge ◽  
Proximal Tubular Dysfunction ◽  
Proximal Tubular

scholarly journals Rickets with hypophosphatemia, hypokalemia and normal anion gap metabolic acidosis: not always an easy diagnosis

2020 ◽  
Vol 13 (1) ◽  
pp. e233350
Author(s):  
Saurav Shishir Agrawal ◽  
Chandan Kumar Mishra ◽  
Chhavi Agrawal ◽  
Partha Pratim Chakraborty
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Potassium Citrate ◽  
Anion Gap ◽  
Tubular Dysfunction ◽  
Diagnostic Challenge ◽  
Primary Defect ◽  
Proximal Tubular Dysfunction ◽  
Proximal Tubular ◽  
Renal Tubular

Rickets other than those associated with advanced kidney disease, isolated distal renal tubular acidosis (dRTA) and hypophosphatasia (defective tissue non-specific alkaline phosphatase) are associated with hypophosphatemia due to abnormal proximal tubular reabsorption of phosphate. dRTA, however, at times is associated with completely reversible proximal tubular dysfunction. On the other hand, severe hypophosphatemia of different aetiologies may also interfere with both distal tubular acid excretion and proximal tubular functions giving rise to transient secondary renal tubular acidosis (distal and/or proximal). Hypophosphatemia and non-anion gap metabolic acidosis thus pose a diagnostic challenge occasionally. A definitive diagnosis and an appropriate management of the primary defect results in complete reversal of the secondary abnormality. A child with vitamin D resistant rickets was thoroughly evaluated and found to have primary dRTA with secondary proximal tubular dysfunction in the form of phosphaturia and low molecular weight proteinuria. The child was treated only with oral potassium citrate. A complete clinical, biochemical and radiological improvement was noticed in follow-up.

scholarly journals Proximal tubular dysfunction and kidney injury associated with tenofovir in HIV patients: a case series

2015 ◽  
Vol 8 (4) ◽  
pp. 420-425 ◽  
Author(s):  
Sana Waheed ◽  
Doaa Attia ◽  
Michelle M. Estrella ◽  
Yousuf Zafar ◽  
Mohamed G. Atta ◽  
...  
Keyword(s):  
Case Series ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Hiv Patients ◽  
Proximal Tubular Dysfunction ◽  
Proximal Tubular

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 The growing pains of ifosfamide

2020 ◽  
Vol 13 (4) ◽  
pp. 500-503 ◽  
Author(s):  
Ben Sprangers ◽  
Sebastian Lapman
Keyword(s):  
Estimated Glomerular Filtration Rate ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Concomitant Treatment ◽  
Proximal Tubular Dysfunction ◽  
French Study ◽  
Growing Pains ◽  
Proximal Tubular

Abstract Ifosfamide is a commonly used chemotherapeutic known to have numerous adverse kidney manifestations. In this issue of Clinical Kidney Journal, Ensergueix et al. report a multicentric observational retrospective French study on 34 adult patients with tubular dysfunction and /or kidney dysfunction following ifosfamide treatment. Of these patients, 18% had isolated proximal tubular dysfunction, 14% had isolated acute kidney injury (AKI), 18% had isolated chronic kidney disease (CKD) and 50% had a combination of proximal tubular dysfunction and AKI. Concomitant treatment with cisplatin was identified as a risk factor for the development of AKI, and cisplatin and age were associated with estimated glomerular filtration rate at last follow-up. Interestingly, the cumulative dose of ifosfamide was not associated with renal outcomes. This report highlights the need for additional studies on the prevalence, spectrum and management of ifosfamide-associated nephrotoxicity and clearly demonstrates that patients who received ifosfamide should be followed long term to detect proximal tubular dysfunction and CKD early.

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.

scholarly journals Proximal tubule-specific overexpression of netrin-1 suppresses acute kidney injury-induced interstitial fibrosis and glomerulosclerosis through suppression of IL-6/STAT3 signaling

2013 ◽  
Vol 304 (8) ◽  
pp. F1054-F1065 ◽  
Author(s):  
Punithavathi Ranganathan ◽  
Calpurnia Jayakumar ◽  
Ganesan Ramesh
Keyword(s):  
Acute Kidney Injury ◽  
Epithelial Cells ◽  
Interstitial Fibrosis ◽  
Kidney Injury ◽  
Transgenic Animals ◽  
Acute Injury ◽  
Tubular Epithelial Cells ◽  
Wild Type ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular

Acute kidney injury-induced organ fibrosis is recognized as a major risk factor for the development of chronic kidney disease, which remains one of the leading causes of death in the developed world. However, knowledge on molecules that may suppress the fibrogenic response after injury is lacking. In ischemic models of acute kidney injury, we demonstrate a new function of netrin-1 in regulating interstitial fibrosis. Acute injury was promptly followed by a rise in serum creatinine in both wild-type and netrin-1 transgenic animals. However, the wild-type showed a slow recovery of kidney function compared with netrin-1 transgenic animals and reached baseline by 3 wk. Histological examination showed increased infiltration of interstitial macrophages, extensive fibrosis, reduction of capillary density, and glomerulosclerosis. Collagen IV and α-smooth muscle actin expression was absent in sham-operated kidneys; however, their expression was significantly increased at 2 wk and peaked at 3 wk after reperfusion. These changes were reduced in the transgenic mouse kidney, which overexpresses netrin-1 in proximal tubular epithelial cells. Fibrosis was associated with increased expression of IL-6 and extensive and chronic activation of STAT3. Administration of IL-6 exacerbated fibrosis in vivo in wild-type, but not in netrin-1 transgenic mice kidney and increased collagen I expression and STAT3 activation in vitro in renal epithelial cells subjected to hypoxia-reoxygenation, which was suppressed by netrin-1. Our data suggest that proximal tubular epithelial cells may play a prominent role in interstitial fibrosis and that netrin-1 could be a useful therapeutic agent for treating kidney fibrosis.

scholarly journals Phycobiliproteins and phycocyanin of Arthrospira maxima (Spirulina) reduce apoptosis promoters and glomerular dysfunction in mercury-related acute kidney injury

2018 ◽  
Vol 2 ◽  
pp. 239784731880507 ◽  
Author(s):  
Placido Rojas-Franco ◽  
Margarita Franco-Colín ◽  
María Estela Meléndez Camargo ◽  
María Mirian Estévez Carmona ◽  
María del Rocío Elizabeth Ortíz-Butrón ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Inorganic Mercury ◽  
Kidney Injury ◽  
Cellular Damage ◽  
Tubular Dysfunction ◽  
Arthrospira Maxima ◽  
Damage Process ◽  
Apoptosis Process ◽  
Nephroprotective Effect

Arthrospira maxima ( Spirulina) is considered a nutraceutical or functional food because it provides health benefits and it is used as nephroprotector because it contains nucleophilic compounds as phycobiliproteins and phycocyanin that prevent oxidative stress and cellular damage process. Also, it is known that inorganic mercury is bioaccumulated and exerted kidney toxicity. Despite the nephroprotective effect of Spirulina and its components, there is not enough information about the effect of them on renal function as well as the apoptosis process inhibition. This work aimed to investigate whether phycobiliproteins and phycocyanin of Spirulina can improve HgCl2-related glomerular and tubular renal dysfunction as well as the Bax, Bcl2, and effectors caspases alterations. Male mice were administrated with Spirulina, phycobiliproteins or phycocyanin 30 min before 5 mg/Kg HgCl2 administration. The nutraceuticals were administrated for the next 5 days. Then, the mice were euthanized. The renal function, caspases 3 and 9 activities, as well as Bax and Bcl2 expression were evaluated. Spirulina and its components prevent HgCl2-related apoptosis induction and glomerular dysfunction. We concluded that phycobiliproteins and phycocyanin of Spirulina reduce glomerular damage but not the tubular dysfunction in a mercury-related acute kidney injury.

scholarly journals Renalase and Biomarkers of Contrast-Induced Acute Kidney Injury

2015 ◽  
Vol 6 (1) ◽  
pp. 25-36 ◽  
Author(s):  
Maciej T. Wybraniec ◽  
Katarzyna Mizia-Stec
Keyword(s):  
Acute Kidney Injury ◽  
Renal Injury ◽  
Amine Oxidase ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Creatinine Concentration ◽  
Invasive Cardiology ◽  
Proximal Tubular ◽  
Novel Biomarkers

Background: Contrast-induced acute kidney injury (CI-AKI) remains one of the crucial issues related to the development of invasive cardiology. The massive use of contrast media exposes patients to a great risk of contrast-induced nephropathy and chronic kidney disease development, and increases morbidity and mortality rates. The serum creatinine concentration does not allow for a timely and accurate CI-AKI diagnosis; hence numerous other biomarkers of renal injury have been proposed. Renalase, a novel catecholamine-metabolizing amine oxidase, is synthesized mainly in proximal tubular cells and secreted into urine and blood. It is primarily engaged in the degradation of circulating catecholamines. Notwithstanding its key role in blood pressure regulation, renalase remains a potential CI-AKI biomarker, which was shown to be markedly downregulated in the aftermath of renal injury. In this sense, renalase appears to be the first CI-AKI marker revealing an actual loss of renal function and indicating disease severity. Summary: The purpose of this review is to summarize the contemporary knowledge about the application of novel biomarkers of CI-AKI and to highlight the potential role of renalase as a functional marker of contrast-induced renal injury. Key Messages: Renalase may constitute a missing biochemical link in the mutual interplay between kidney and cardiac pathology known as the cardiorenal syndrome.

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