scholarly journals MO166AUTOPTIC KIDNEY FINDINGS IN HOSPITALIZED PATIENTS WITH COVID-19

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Giulio Nobile ◽  
Simone Nicoletti ◽  
Marisa Santostefano
Keyword(s):  
Renal Failure ◽  
Light Microscopy ◽  
Acute Tubular Necrosis ◽  
Cytopathic Effect ◽  
Diffuse Alveolar Damage ◽  
Kidney Damage ◽  
Rt Pcr ◽  
Tubular Necrosis ◽  
Obesity And Diabetes ◽  
Lung Failure

Abstract Background and Aims SARS-CoV-2, isolated for the first time at the end of 2019, is the third human infecting Coronavirus found so far. Acute kidney injury (AKI) is the most common presentation when kidney is involved. There is evidence that kidney damage is determined through different pathological mechanisms. Has been observed that pathological kidney lesions can be due to the direct cytopathic effect of the virus on tubular cells or by pro-inflammatory cytokine storm. Aim of this observation is to evaluate the clinical and pathological patterns of kidney damage mediated by Coronavirus. Method We analysed kidney autopsies of 4 patients with COVID-19 infection, hospitalized between March and April 2020, admitted to the Intensive Care Unit. The tissue samples have been observed by light microscopy and immunofluorescence. RT-PCR SARS-CoV-2 was performed in all cases. Results Case 1 female, 69 y; affected by obesity, previous ictus; smoking habit. Admitted for COVID-related pneumonia. At onset creatinine 0.45 mg/dl. Progression of lung failure and exitus after 3 days. Autopsy: diffuse alveolar damage. Renal autopsy: acute tubular necrosis; mild glomerular ischemia, lymphocyte T CD4+ parenchyma infiltration. Case2 male, 66 y; affected by hypertension with cardiac involvement. Admitted for persistent fever. At onset creatinine 0.98 mg/dl. Nasopharingeal swab COVID-19 positive. Progression of lung failure and oligoanuric AKIn 3 (creatinine 4.5 mg/dl, urea 239 mg/dl), dialysis dependent. Exitus after one week for diffuse alveolar damage and sepsis. Renal autopsy: proximal and distal acute tubular moderate injury, mild diffuse glomerular ischemia, glomerular capillaritis, overlap chronic nephropathy. Case 3 male 45 y; affected by obesity and diabetes. Admitted for COVID-related pneumonia with acute lung failure requiring ECMO. After one week developed AKIn 3 dialysis dependent. Exitus for cardio-respiratory arrest. Renal autopsy: diffuse acute tubular necrosis, glomerular capillaritis, overlap chronic diabetic nephropathy. Case 4 male, 51 y; affected by CKD grade IV, hypertension, previous ictus; drug abuser. Admitted for AKIn 2 and COVID-related pneumonia. After 3 days progression of lung and renal failure requiring intubation and dialysis treatment. Exitus the day after for diffusive alveolar damage and lymphocytic myocarditis. Renal autopsy: diffused acute tubular necrosis, glomerular ischemia with mild tuft collapsing, diffuse infiltration of lymphocytes CD4+. In all cases light microscopy examination showed diffuse proximal tubular injury, with isomeric and non-isomeric vacuolar degeneration; collapsing tuft, and interstitial inflammation. Virus RNA performed by RT-PCR on kidney tissue was positive in all patients. Moreover in some cases our patients showed multi-systemic organ involvement: lung in 4 cases, heart in 1, liver in 1. Conclusion Our observations show that the main pathological effect caused by Coronavirus is a direct cytopathic effect on the proximal tubules with variable degree of damage until acute tubular necrosis (ATN). In addition to this pathway, other factors contributing to kidney damage include systemic hypoxia, microvascular capillaritis. Associated sepsis can worse overall and renal survival. Previous comorbidities, especially obesity, diabetes, systemic hypertension and preexisting chronic renal failure, are significant negative prognostic factors.

Acute Tubular Necrosis: Diagnosis, Treatment, and Nursing Implications

1992 ◽  
Vol 3 (3) ◽  
pp. 688-697
Author(s):  
Sara Douglas
Keyword(s):  
At Risk ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Critical Care ◽  
Acute Tubular Necrosis ◽  
Early Recognition ◽  
Recovery Phase ◽  
Vital Role ◽  
Laboratory Findings ◽  
Tubular Necrosis

Acute tubular necrosis (ATN) is the most common cause of acute renal failure. Early recognition of patients who are at risk for ATN can prevent or improve the course of ATN. Acute renal failure is classified as prerenal, intrinsic, or postrenal disease. ATN is classified as a type of intrinsic renal disease. The clinical course of ATN is divided into the renal failure phase, diuretic phase, and recovery phase, with each phase having distinct symptoms and laboratory findings. Diagnosis of ATN often is complicated and confusing; understanding of laboratory findings can facilitate the critical care nurse’s ability to assess those at risk for ATN. The care and treatment of the patient with ATN is complicated, and specific treatments are discussed in detail. The critical care nurse can play a vital role in identifying the patient at risk, preventing the development of ATN in those at risk, and providing appropriate care for those who develop ATN

scholarly journals Management of Acute Renal Failure

1972 ◽  
Vol 1 (1) ◽  
pp. 65-69 ◽  
Author(s):  
J. M. Hayes
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Acute Tubular Necrosis ◽  
Urinary Tract Obstruction ◽  
Renin Angiotensin System ◽  
Sodium Concentration ◽  
Therapeutic Trial ◽  
Angiotensin System ◽  
Tubular Necrosis ◽  
Occlusive Vascular Disease

Acute renal failure has oliguria and uraemia as its cardinal manifestations. The syndrome may be due to acute tubular necrosis, glomerulonephritis, urinary tract obstruction and occlusive vascular disease. The renal damage due to acute tubular necrosis is of uncertain aetiology. Renal cortical ischaemia and depression of glomerular filtration rate are important in the pathogenesis. Activation of the renin-angiotensin system and glomerular coagulation may prove to be important in these changes. The differentiation between reversible oliguria and established renal failure is generally accomplished on clinical grounds and the response to a therapeutic trial of mannitol. Measurement of urinary sodium concentration and osmolality are valuable adjuncts. The keystone of management is the prevention of symptomatic uraemia. Infection and haemorrhage have now replaced pulmonary oedema and hyperkalaemia as the major causes of death. The mortality rate remains high in acute tubular necrosis and a significant mortality occurs in the diuretic phase.

IgA Nephropathy: Acute Renal Failure, Acute Tubular Necrosis, and Features of Postinfectious Acute Glomerulonephritis

Renal Failure ◽  
1992 ◽  
Vol 14 (4) ◽  
pp. 533-539 ◽  
Author(s):  
Helga Maria Mazzarolo-Cruz ◽  
Décio de Oliveira Penna ◽  
Luis Balthazar Saldanha ◽  
Elza Hissako Kanashiro ◽  
Jenner Cruz ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Iga Nephropathy ◽  
Acute Tubular Necrosis ◽  
Acute Glomerulonephritis ◽  
Tubular Necrosis

scholarly journals Renal and Electrolyte Abnormalities in Heat Stroke during Hajj

2011 ◽  
Vol 1 (2) ◽  
pp. 33-35
Author(s):  
Rana A. Nabalawi
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Acute Tubular Necrosis ◽  
Heat Stroke ◽  
Respiratory Alkalosis ◽  
Summer Period ◽  
Dry Skin ◽  
Systemic Complications ◽  
Tubular Necrosis ◽  
Electrolyte Abnormalities

Background: Heat induced illnesses are variable from a mild heat exhaustion to a severe heat stroke and its systemic complications. Millions of pilgrims annually perform the Islamic obligatory mission of Hajj, are vulnerable to heat induced illnesses, especially when Hajj falls in the summer period. This is a retrospective study of the renal and electrolyte abnormalities in heat stroke patients during Hajj. Method: We selected randomly 472 patients out of 2044 patients diagnosed as heat stroke over 5 years from 1986-1991 for this study. The diagnosis of heat stroke was based on: 1) Rectal temperature > 40°C, 2) Hot dry skin and 3) Neurological deficit presenting as delirium, coma with or without convulsions. The renal function and electrolytes of all these patients were obtained. Results: All the 472 patients revealed significant electrolyte abnormalities: hypophasphatemia 98% (P + 0.55 ± 0.05 mmol/L), hyponatremia Na+ 70% (128 + 1 mmol/L), hypocalcemia 70% (Ca + 2.01 ± 0.02 mmol/L), hypokalemia 32% (K+3.3 ± 01 mmol/L), and hypomagnesaemia (Mg 0.06 ± 0.01 mmol/L) in 30%. Metabolic acidosis and compensatory respiratory alkalosis was seen in most patients. Acute renal failure that required dialysis developed in 180 (8.8%) patients. In 100 patients, the most common cause was Rhabdomyolysis (68%). The rest had ischemic acute tubular necrosis (32%) with a mortality of 15% compared to 20% in all the 472 patients. The risk mortality was higher in patients with a temperature of 42°C, comatose at presentation and older than 50 years. Conclusion: During Hajj, electrolyte abnormalities in heat stroke were found to be fairly common. Acute renal failure was mainly due to Rhabdomyolysis, which carry better prognosis compared to other causes of acute tubular necrosis.

scholarly journals Drug-induced acute tubular necrosis

2020 ◽  
pp. 49-62
Author(s):  
O.D. Ostroumova ◽  
◽  
M.V. Klepikova ◽  
K.K. Dzamikhov ◽  
V.A. De ◽  
...  
Keyword(s):  
Risk Factors ◽  
Acute Tubular Necrosis ◽  
Kidney Damage ◽  
Drug Induced ◽  
Main Method ◽  
Tubular Necrosis ◽  
Risk Of Mortality ◽  
History Of ◽  
Nephrotoxic Drugs ◽  
Management Schemes

Nowadays, there is an increasing necessity to use a lot of medical products (MP) in one patient. This can lead to potential nephrotoxic adverse reactions (ADRs) among drugs. One of drug-induced kidney damage manifestations is acute tubular necrosis (ATN), which causes the development of severe complications associated with the use of hemodialysis and a high risk of mortality. The purpose of this review is to analyze literature data concerning groups of drugs and individual drugs, the intake of which is associated with the development of drug-induced ATN, risk factors, prevention and treatment methods. Among drug-induced ATN development risk factors are both general, associated with the development of drug-induced acute kidney damage (for example, age, history of chronic kidney disease, etc.), and specific ones, typical for certain groups of drugs. Most often, drug-induced ATN develops while taking antibacterial, antiviral and anticancer drugs. The main method of treatment for drug-induced ATN is abolition of nephrotoxic drugs, but if it is impossible, then there are certain patient management schemes. To prevent and to diagnose drug-induced ATN at early stages, that is the key for favorable prognosis, it is necessary to aware of doctors of different specialties about such pharmacotherapy complications.

scholarly journals Syndrome of flank pain and acute renal failure after binge drinking and nonsteroidal anti-inflammatory drug ingestion.

1995 ◽  
Vol 5 (9) ◽  
pp. 1647-1652
Author(s):  
G R Johnson ◽  
S F Wen
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Binge Drinking ◽  
Acute Tubular Necrosis ◽  
Extracellular Volume ◽  
Renal Perfusion ◽  
Flank Pain ◽  
Inflammatory Drug ◽  
Tubular Necrosis ◽  
Anti Inflammatory

The binge drinking of alcohol combined with the ingestion of a nonsteroidal anti-inflammatory drug (NSAID) is a recently described cause of reversible acute renal failure. The pathogenetic mechanisms leading to acute tubular necrosis in this setting include the initial compromise in renal perfusion due to alcohol-induced extracellular volume contraction and the superimposed renal hemodynamic alterations induced by the NSAID that interfere with the renal autoregulation. Although alcohol may also cause rhabdomyolysis leading to acute tubular necrosis, this is usually not apparent in these cases. Previously, only three such cases have been reported but the incidence is likely to be higher in view of the prevalence of alcohol and NSAID use. Herein is presented another patient in whom the features of flank pain and acute renal failure in association with binge drinking and NSAID ingestion constitute a characteristic syndrome.

scholarly journals P. falciparum Malaria induced Renal impairment

2019 ◽  
Vol 5 (6) ◽  
pp. 220-223
Author(s):  
Tarkeswar Aich ◽  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Renal Dysfunction ◽  
Falciparum Malaria ◽  
Acute Tubular Necrosis ◽  
Mean Value ◽  
Intravascular Haemolysis ◽  
Tubular Necrosis ◽  
Oliguric Renal Failure

Introduction: The involvement of the kidney in falciparum malaria has been known for decades. In 1944, Spitz observed acute renal failure due to falciparum infection in soldiers during World War II. This observation was later supported by other workers who detected oliguria developing in patients with black water fever. The initial clinical pattern is that of reversible renal dysfunction or pre-renal azotemia, which rapidly progresses to acute tubular necrosis if treatment is not started early. Patients with malaria induced renal failure are hypercatabolic with blood urea and serum creatinine levels rising rapidly.Oliguric as well non-oliguric renal failure are observed and duration of oliguric renal failure ranges from a few days to several weeks depending on the severity of renal dysfunction. Acute renal failure in falciparum malaria is usually associated either with acute intravascular haemolysis or heavy parasitemia. Acute renal failure in falciparum malaria is also observed in patients with severe intravascular haemolysis resulting in haemoglobinuria. It may be induced by malarial fever or by anti-malarial drugs in a patient with or without G6-PD deficiency. Materials and Methods: This is a hospital based cross sectional study carried out in a total of 50 cases of acute renal failure who were selected from diagnosed patients of P. falciparum malaria. Cases were confirmed either by P. falciparum antigen test and/or peripheral blood smear test(both thick and thin smear).Malarial ARF (MARF) is diagnosed when serum creatinine level > 3 mg/dl, and/or urine output < 400 ml/24hrs despite adequate rehydration. Result: Out of 174 cases of falciparum malaria 50 patients (28.7%) had acute renal failure in falciparum malaria. 36 (72%) cases were males and 14 (28%) were females, indicating a much higher incidence in males. Approximately 78% of the cases in the present study were below the age of 40 years. The youngest was 15 years old and the oldest was 61 years old (Mean age – 32 ± 11.6 years). All were febrile (100%) and a majority had oliguria or anuria (72%); jaundice was detected in 30 (60%) patients on presentation. Hepatomegaly & Splenomegaly were found in 76% & 66% of the cases respectively. Out of the total 50 cases of malaria induced ARF, 14 cases (28%) had pre-renal ARF while in the majority, 72% the clinical course was that of ATN. The pathogenesis of ATN in the 36 cases was found to be heavy parasitaemia in 40% of the cases, IV hemolysis with haemoglobinuria in 3 (6%) of cases; and cholestatic jaundice in 26% of falciparum patients. Examination of the urinary sediments revealed that albumin was present in urine in 40 cases (80%). Majority of the patients had significant rise in blood urea level with a mean value of 177 mg. S. creatinine levels ranged between 3.2 - 13.6 mg with a mean value of 7.83 mg. The mean creatinine clearance rate was 11.71 ml/min. The overall mortality rate was 26%. Conclusion: AKI is common in Falciparum malaria. The pathogenesis of AKI is largely unknown but may be related to the erythrocyte sequestration and agglutination within the renal microcirculation interfering with flow and metabolism. Clinically and pathologically, this syndrome manifests as Pre-renal azotemia and acute tubular necrosis. Acute renal failure may occur simultaneously with other vital-organ dysfunction (in which case the mortality risk is high) or may progress as other disease manifestations resolve. Early dialysis or hemofiltration considerably enhances the likelihood of a patient’s survival, particularly in acute hypercatabolic renal failure. Severity of oliguria and presence of one or more associated complications like pulmonary oedema, acidosis, and altered sensorium have considerable influence on the outcome of the patients.

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.

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