scholarly journals Urinary cytology as a tool for differential diagnosis between acute tubular necrosis and proliferative glomerulonephritis in patients with nephrotic syndrome and acute kidney injury

2020 ◽  
Author(s):  
Caroline Vilas Boas de Melo ◽  
Maria Brandão Tavares ◽  
Paula Neves Fernandes ◽  
Carlos Alberto Santos Silva ◽  
Ricardo David Couto ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Differential Diagnosis ◽  
Nephrotic Syndrome ◽  
Acute Tubular Necrosis ◽  
Rapidly Progressive Glomerulonephritis ◽  
Kidney Injury ◽  
Small Cells ◽  
Urinary Cytology ◽  
Glomerular Lesion ◽  
Tubular Necrosis

Abstract Objective Acute tubular necrosis (ATN) is a frequent cause of acute kidney injury (AKI). In patients with nephrotic syndrome (NS), AKI demands the differential diagnosis between ATN and rapidly progressive glomerulonephritis. In some cases, conclusive diagnosis is possible only by kidney biopsy. We aimed to study the potential use of urine cytology in the differential diagnosis between ATN and proliferative glomerular lesion in patients with NS.Results Cell size analysis showed a higher proportion of small cells and a lower proportion of large cells in the urine of patients with AKI. Cells phenotypes were easily defined using cytological preparations. Leukocytes were found to be a primary classifier of NS groups, with higher number in patients with AKI and patients with proliferative glomerular lesions. Our data suggests that urinary cytology can be readily performed and support the differential diagnosis between proliferative glomerular lesion and ATN in patients with NS and AKI.

scholarly journals Biomarkers of acute kidney injury in patients with nephrotic syndrome

2020 ◽  
Author(s):  
Maria Brandão Tavares ◽  
Caroline Vilas Boas de Melo ◽  
Paula Neves Fernandes ◽  
Maria da Conceição Chagas de Almeida ◽  
Marcia Fernanda dos Santos Melo Carneiro ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Nephrotic Syndrome ◽  
Acute Tubular Necrosis ◽  
Kidney Injury ◽  
Proliferative Glomerulonephritis ◽  
Cross Sectional ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Tubular Necrosis ◽  
Kidney Injury Molecule 1 ◽  
Neutrophil Gelatinase

ABSTRACT Introduction: Emergence of acute kidney injury (AKI) in patients with nephrotic syndrome (NS) requires prompt diagnosis and differentiation between acute tubular necrosis (ATN) and proliferative glomerulonephritis. We studied the potential use of commercial urinary biomarkers' tests in the diagnosis of AKI in patients with NS. Methods: A cross sectional estimate of urinary concentrations of KIM-1 and NGAL was performed in 40 patients with NS: 9 with proliferative glomerulopathy, being 4 with AKI and 31 without proliferative glomerulopathy, being 15 with AKI. AKI was defined using the KDIGO criteria. Results: The mean age was 35 ± 16 years. The main diagnoses were focal and segmental glomerulosclerosis (10, 25%), membranous glomerulopathy (10, 25%), minimal change disease (7, 18%), lupus nephritis (6, 15%), and proliferative glomerulonephritis (3, 8%). Patients with ATN had higher levels of urinary KIM-1 (P = 0.0157) and NGAL (P = 0.023) than patients without ATN. The urinary concentrations of KIM-1 (P= 0.009) and NGAL (P= 0.002) were higher in patients with AKI than in patients without AKI. Urinary NGAL and KIM-1 levels were significantly higher in patients with ATN without proliferative glomerulonephritis than in patients with proliferative glomerulonephritis (P = 0.003 and P=0.024, respectively). Conclusions: Neutrophil gelatinase associated lipocalin (NGAL) and kidney injury molecule 1 (KIM-1) estimates correlated with histological signs of ATN and were able to discriminate patients with AKI even in conditions of NS. Furthermore, urinary levels of NGAL and KIM-1 may be useful in the differential diagnosis of acute tubular necrosis and exudative glomerulonephritis in patients with nephrotic syndrome.

scholarly journals Urinary cytology: a potential tool for differential diagnosis of acute kidney injury in patients with nephrotic syndrome

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Caroline Vilas Boas de Melo ◽  
Maria Brandão Tavares ◽  
Paula Neves Fernandes ◽  
Carlos Alberto dos Santos Silva ◽  
Ricardo David Couto ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Differential Diagnosis ◽  
Nephrotic Syndrome ◽  
Kidney Injury ◽  
Urinary Cytology ◽  
Potential Tool

scholarly journals Prognosis of Acute Kidney Injury and Hepatorenal Syndrome in Patients with Cirrhosis: A Prospective Cohort Study

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Andrew S. Allegretti ◽  
Guillermo Ortiz ◽  
Julia Wenger ◽  
Joseph J. Deferio ◽  
Joshua Wibecan ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cohort Study ◽  
Prospective Cohort Study ◽  
Acute Tubular Necrosis ◽  
Prospective Cohort ◽  
Hepatorenal Syndrome ◽  
Kidney Injury ◽  
Multicenter Studies ◽  
Urinary Sediment ◽  
Tubular Necrosis

Background/Aims. Acute kidney injury is a common problem for patients with cirrhosis and is associated with poor survival. We aimed to examine the association between type of acute kidney injury and 90-day mortality.Methods. Prospective cohort study at a major US liver transplant center. A nephrologist’s review of the urinary sediment was used in conjunction with the 2007 Ascites Club Criteria to stratify acute kidney injury into four groups: prerenal azotemia, hepatorenal syndrome, acute tubular necrosis, or other.Results. 120 participants with cirrhosis and acute kidney injury were analyzed. Ninety-day mortality was 14/40 (35%) with prerenal azotemia, 20/35 (57%) with hepatorenal syndrome, 21/36 (58%) with acute tubular necrosis, and 1/9 (11%) with other (p=0.04overall). Mortality was the same in hepatorenal syndrome compared to acute tubular necrosis (p=0.99). Mortality was lower in prerenal azotemia compared to hepatorenal syndrome (p=0.05) and acute tubular necrosis (p=0.04). Ten participants (22%) were reclassified from hepatorenal syndrome to acute tubular necrosis because of granular casts on urinary sediment.Conclusions. Hepatorenal syndrome and acute tubular necrosis result in similar 90-day mortality. Review of urinary sediment may add important diagnostic information to this population. Multicenter studies are needed to validate these findings and better guide management.

Continuous Peritoneal Dialysis Compared with Daily Hemodialysis in Patients with Acute Kidney Injury

2009 ◽  
Vol 29 (2_suppl) ◽  
pp. 62-71 ◽  
Author(s):  
Daniela Ponce Gabriel ◽  
Jacqueline Teixeira Caramori ◽  
Luis Cuadrado Martin ◽  
Pasqual Barretti ◽  
Andre Luis Balbi
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Peritoneal Dialysis ◽  
Survival Rate ◽  
Acute Tubular Necrosis ◽  
Kidney Injury ◽  
Acid Base ◽  
Tubular Necrosis ◽  
Daily Hemodialysis ◽  
Continuous Peritoneal Dialysis

Background In some parts of the world, peritoneal dialysis is widely used for renal replacement therapy (RRT) in acute kidney injury (AKI), despite concerns about its inadequacy. It has been replaced in recent years by hemodialysis and, most recently, by continuous venovenous therapies. We performed a prospective study to determine the effect of continuous peritoneal dialysis (CPD), as compared with daily hemodialysis (dHD), on survival among patients with AKI. Methods A total of 120 patients with acute tubular necrosis (ATN) were assigned to receive CPD or dHD in a tertiary-care university hospital. The primary endpoint was hospital survival rate; renal function recovery and metabolic, acid–base, and fluid controls were secondary endpoints. Results Of the 120 patients, 60 were treated with CPD (G1) and 60 with dHD (G2). The two groups were similar at the start of RRT with respect to age (64.2 ± 19.8 years vs 62.5 ± 21.2 years), sex (men: 72% vs 66%), sepsis (42% vs 47%), shock (61% vs 63%), severity of AKI [Acute Tubular Necrosis Individual Severity Score (ATNISS): 0.68 ± 0.2 vs 0.66 ± 0.22; Acute Physiology and Chronic Health Evaluation (APACHE) II: 26.9 ± 8.9 vs 24.1 ± 8.2], pre-dialysis blood urea nitrogen [BUN (116.4 ± 33.6 mg/dL vs 112.6 ± 36.8 mg/dL)], and creatinine (5.85 ± 1.9 mg/dL vs 5.95 ± 1.4 mg/dL). In G1, weekly delivered Kt/V was 3.59 ± 0.61, and in G2, it was 4.76 ± 0.65 ( p < 0.01). The two groups were similar in metabolic and acid–base control (after 4 sessions, BUN < 55 mg/dL: 46 ± 18.7 mg/dL vs 52 ± 18.2 mg/dL; pH: 7.41 vs 7.38; bicarbonate: 22.8 ± 8.9 mEq/L vs 22.2 ± 7.1 mEq/L). Duration of therapy was longer in G2 (5.5 days vs 7.5 days; p = 0.02). Despite the delivery of different dialysis methods and doses, the survival rate did not differ between the groups (58% in G1 vs 52% in G2), and recovery of renal function was similar (28% vs 26%). Conclusion High doses of CPD provided appropriate metabolic and pH control, with a rate of survival and recovery of renal function similar to that seen with dHD. Therefore, CPD can be considered an alternative to other forms of RRT in AKI.

When acute kidney injury in the intensive care unit is not acute tubular necrosis: A case report of κ-light chain crystalline tubulopathy

2019 ◽  
Vol 91 (5) ◽  
pp. 311-316
Author(s):  
Neal Shah ◽  
Ivy Rosales ◽  
Rex Neal Smith ◽  
Jacob E. Berchuck ◽  
Andrew J. Yee ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Acute Kidney Injury ◽  
Intensive Care ◽  
Case Report ◽  
Light Chain ◽  
Acute Tubular Necrosis ◽  
Kidney Injury ◽  
Tubular Necrosis

scholarly journals MO134COVID-19-ASSOCIATED KIDNEY INJURY IS CHARACTERIZED BY ACUTE TUBULAR NECROSIS AND CAPILLARY CONGESTION WITH EVIDENCE FOR SARS-COV-2 IN THE NEPHRON

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Antoine Bouquegneau ◽  
Pauline Erpicum ◽  
Stéphanie Grosch ◽  
Lionel Habran ◽  
Olivier Hougrand ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Acute Kidney Injury ◽  
In Situ Hybridization ◽  
Acute Tubular Necrosis ◽  
Kidney Injury ◽  
Post Mortem ◽  
Rt Pcr ◽  
N Protein ◽  
Tubular Necrosis

Abstract Background and Aims Kidney damage has been reported in COVID-19 patients. Despite numerous reports about COVID-19-associated nephropathy, the factual presence of the SARS-CoV-2 in the renal parenchyma remains controversial. Method We consecutively performed 16 immediate (≤3h) post-mortem renal biopsies in patients diagnosed with COVID-19. Kidney samples from 5 patients who died from sepsis and were free from COVID-19 were used as controls. Samples were methodically evaluated by 3 pathologists. Virus detection in the renal parenchyma was performed in all samples by bulk RNA RT-PCR (E and N1/N2 genes), immunostaining (nCoV2019 N-Protein), fluorescent in situ hybridization (nCoV2019-S) and electron microscopy. Results The mean age of our COVID-19 cohort was 68.2±12.8 years, most of whom were males (68.7%). Proteinuria was observed in 53.3% of cases, while acute kidney injury occurred in 60% of cases. Acute tubular necrosis of variable severity was found in all cases, with no tubular or interstitial inflammation. There was no difference in acute tubular necrosis severity between the patients with COVID-19 versus control samples. Congestion in glomerular and peri-tubular capillaries was respectively observed in 56.3 and 87.5% of patients with COVID-19 compared to 20% of controls, with no evidence of thrombi. The nCoV2019 N-Protein was detected in proximal tubules and also at the basolateral pole of scattered cells of the distal tubules in 9/16 cases. In situ hybridization confirmed these findings. RT-PCR of kidney total RNA detected SARS-CoV-2 N gene in one case. Electron microscopy did not show typical viral inclusions. Conclusion Our immediate post-mortem kidney samples from patients with COVID-19 highlight a congestive pattern of acute kidney injury, with no significant glomerular or interstitial inflammation. Immunostaining and in situ hybridization suggest that SARS-CoV-2 is present in various segments of the nephron.

scholarly journals Biopsy-Proven Acute Tubular Necrosis due to Vancomycin Toxicity

2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Farheen Shah-Khan ◽  
Marc H. Scheetz ◽  
Cybele Ghossein
Keyword(s):  
Acute Kidney Injury ◽  
Interstitial Nephritis ◽  
Acute Tubular Necrosis ◽  
Kidney Injury ◽  
Acute Interstitial Nephritis ◽  
Etiologic Factor ◽  
Clinical Use ◽  
Tubular Necrosis

Vancomycin (VAN) has been associated with acute kidney injury (AKI) since it has been put into clinical use in the 1950's. Early reports of AKI were likely linked to the impurities of the VAN preparation. With the advent of the more purified forms of VAN, the incidence of AKI related to VAN were limited to acute interstitial nephritis (AIN) or as a potentiating agent to other nephrotoxins such as Aminoglycosides. VAN as the sole etiologic factor for nephrotoxic acute tubular necrosis (ATN) has not been described. Here, we report a case of biopsy-proven ATN resulting from VAN.

scholarly journals Rhabdomyolysis and Acute Kidney Injury Requiring Dialysis as a Result of Concomitant Use of Atypical Neuroleptics and Synthetic Cannabinoids

2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Aiyu Zhao ◽  
Maybel Tan ◽  
Aung Maung ◽  
Moro Salifu ◽  
Mary Mallappallil
Keyword(s):  
Acute Kidney Injury ◽  
Differential Diagnosis ◽  
Adverse Effects ◽  
Serum Creatinine ◽  
Synthetic Cannabinoids ◽  
Kidney Injury ◽  
Atypical Neuroleptics ◽  
Unique Case ◽  
Urine Metabolites ◽  
Tubular Necrosis

The use of synthetic cannabinoids (SCBs) is associated with many severe adverse effects that are not observed with marijuana use. We report a unique case of a patient who developed rhabdomyolysis and acute kidney injury (AKI) requiring dialysis after use of SCBs combined with quetiapine. Causes for the different adverse effects profile between SCBs and marijuana are not defined yet. Cases reported in literature with SCBs use have been associated with reversible AKI characterized by acute tubular necrosis and interstitial nephritis. Recent studies have showed the involvement of cytochromes P450s (CYPs) in biotransformation of SCBs. The use of quetiapine which is a substrate of the CYP3A4 and is excreted (73%) as urine metabolites may worsen the side effect profiles of both quetiapine and K2. SCBs use should be included in the differential diagnosis of AKI and serum Creatinine Phosphokinase (CPK) level should be monitored. Further research is needed to identify the mechanism of SCBs nephrotoxicity.

scholarly journals Prolonged Recovery Time from Zoledronic Acid Induced Acute Tubular Necrosis: A Case Report and Review of the Literature

2013 ◽  
Vol 2013 ◽  
pp. 1-5
Author(s):  
Frederic Rahbari-Oskoui ◽  
Odicie Fielder ◽  
Nima Ghasemzadeh ◽  
Randolph Hennigar
Keyword(s):  
Acute Kidney Injury ◽  
Zoledronic Acid ◽  
Acute Tubular Necrosis ◽  
Recovery Time ◽  
Metastatic Cancer ◽  
Metastatic Breast ◽  
Kidney Injury ◽  
Tubular Necrosis ◽  
Prolonged Recovery ◽  
Caucasian Female

Acute tubular necrosis (ATN) due to bisphosphonates has been reported with Zoledronic acid but the time to recovery (if any) has been usually less than 4 months. Possible recovery time from ATN of any cause is usually less than 6 months. In this paper, we present the case of a 59-year-old Caucasian female with metastatic breast cancer who had received 16 monthly injections of Zoledronic acid for treatment of tumor induced hypercalcemia and developed several episodes of mild acute kidney injury which resolved by withholding treatment. Unfortunately, after the sixteenth injection, the patient experienced severe acute kidney injury, with a peak serum creatinine of 8.0 mg/dL. Although urinalysis showed muddy brown casts, because of atypical recovery time and presence of eosinophiluria and subnephrotic range proteinuria, a kidney biopsy was performed. Diagnosis of typical acute tubular necrosis was confirmed without any other concomitant findings. The course was remarkable for an unusually slow recovery of renal function over 15 months without need for renal replacement therapy until the patient expired from her metastatic cancer two years later. We reviewed all the published cases of acute kidney injury due to Zoledronic acid and suggest recommendations for clinicians and researchers.

scholarly journals Community Acquired Acute Kidney Injury from Edible Agents: Report from a Developing Country, Bangladesh

2017 ◽  
Vol 10 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Tabassum Samad ◽  
Wasim M. Mohosin ul Haque ◽  
Muhammad A. Rahim ◽  
Sarwar Iqbal ◽  
Palash Mitra
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Acute Tubular Necrosis ◽  
Public Awareness ◽  
Kidney Injury ◽  
Energy Drink ◽  
Renal Tubules ◽  
Tubular Necrosis ◽  
Oxalate Crystals ◽  
Star Fruit

Toxin is a common cause of community acquired acute kidney injury (AKI) which includes environmental toxins like plant toxins as well as various drugs and chemicals which are usually ingested for medicinal as well as recreational purposes.Averrhoa carambola(Star fruit/ Kamranga) andAvorrhoa bilimbiare two such commonly used traditional remedies. They belong to familyOxalidaecaeand contain high-levels of oxalic acid. AKI may occur after consuming concentrated juice due to deposition of oxalate crystals in the renal tubules.Here we present two patients who developed AKI after ingestion of freshly made juice from A. bilimbi and star fruit. Both patients were diabetic and the juice was ingested on empty stomach with the belief of improving glycemic status. Initial presentation was GI upset in both scenarios. Patient with A. bilimbi toxicity had diabetic nephropathy and required hemodialysis. Renal biopsy revealed deposition of polarizable oxalate crystals in the patient who consumed A. bilimbi and acute tubular necrosis in the patient with star fruit toxicity. All cases regained normal renal function within three months.We also present a patient who ingested raw fish gallbladder as a remedy for asthma. The patient presented with AKI within five days of ingestion and required hemodialysis. His highest serum creatinine was 10.4mg/dl and fell to 1.7 mg/dl after four weeks. Cyprinol and related compounds in fish gallbladder are thought to be the cause of acute tubular necrosis in such cases.The fourth patient developed AKI with rhabdomyolysis after consuming a locally made energy drink. He also required dialysis and serum creatinine gradually improved from 7.2mg/dl to 1.4mg/dl at discharge. The possibility of toxicity of caffeine, adulteration with other chemicals or ascorbic acid toxicity causing oxalate nephropathy could not be excluded.All four patients developed AKI caused after ingesting easily available products and are presented here for public awareness. We believe proper knowledge and education can reduce toxin induced AKI in our society.

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