scholarly journals Renal hemosiderosis presenting with acute kidney Injury and macroscopic hematuria in Immunoglobulin A nephropathy: a case report

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Shinya Taguchi ◽  
Sumi Hidaka ◽  
Mitsuru Yanai ◽  
Kunihiro Ishioka ◽  
Kenji Matsui ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Biopsy ◽  
Prussian Blue ◽  
Iga Nephropathy ◽  
Acute Tubular Necrosis ◽  
Immunoglobulin A ◽  
Kidney Injury ◽  
Upper Respiratory Tract ◽  
Macroscopic Hematuria ◽  
Tubular Necrosis

Abstract Background Macroscopic hematuria-associated acute kidney injury (AKI) is a well-known complication of immunoglobulin A (IgA) nephropathy. In such cases, intratubular obstruction by red blood cell (RBC) casts and acute tubular necrosis are mainly observed pathologically. Herein, we report the case of a patient with IgA nephropathy presenting with AKI following an episode of macrohematuria. The patient presented with severe renal tubular hemosiderosis and acute tubular necrosis and without any obvious obstructive RBC casts. Case presentation A 68-year-old woman, who was diagnosed with IgA nephropathy on renal biopsy 6 years ago, was admitted to our hospital after an episode of macroscopic glomerular hematuria and AKI following upper respiratory tract infection. Renal biopsy showed mesangial proliferation of the glomeruli, including crescent formation in 17 % of the glomeruli, and acute tubular necrosis without obvious hemorrhage or obstructive RBC casts. The application of Perls’ Prussian blue stain showed hemosiderin deposition in the renal proximal tubular cells. Immunofluorescence showed granular mesangial deposits of IgA and C3. Based on these findings, she was diagnosed with acute tubular necrosis with a concurrent IgA nephropathy flare-up. Moreover, direct tubular injury by heme and iron was considered to be the cause of AKI. She was treated with intravenous pulse methylprednisolone followed by oral prednisolone. Thereafter, the gross hematuria gradually faded, and her serum creatinine levels decreased. Conclusions IgA nephropathy presenting with acute kidney injury accompanied by macrohematuria may cause renal hemosiderosis and acute tubular necrosis without obstructive RBC casts. Hemosiderosis may be a useful indicator for determining the pathophysiology of macroscopic hematuria-associated AKI. However, renal hemosiderosis may remain undiagnosed. Thus, Perls’ Prussian blue iron staining should be more widely used in patients presenting with hematuria.

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 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.

scholarly journals Automobile Paint Reducer Induced Acute Kidney Injury

2021 ◽  
Vol 5 (2) ◽  
pp. 10-13
Author(s):  
Muzamil Latief ◽  
Zhahid Hassan ◽  
Mohd Latief Wani ◽  
Farhat Abbas ◽  
Summyia Farooq
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Organic Solvents ◽  
Acute Tubular Necrosis ◽  
Kidney Injury ◽  
Solvent Exposure ◽  
The Third ◽  
Tubular Necrosis

The various aspects of the automobile industry also carry with it the risk for occupational health hazards with it. Toluene has also evolved as a commonly used drug by substance abusers. Accidental exposure or self-poisoning with these substances has been reported in literature. These substances can also cause distal renal tubular acidosis (RTA), acute tubular necrosis, glomerulonephritis and interstitial nephritis, rhabdomyolysis and myoglobinemia.In this series, we report about three patients who developed renal manifestations because of organic solvents. Two of the three patients had ingested the paint reducer substance and the third one was addicted to sniffing the toluene based paint reducer. All the patients had in taken these substances with suicidal intent and developed acute kidney injury (AKI) and severe metabolic acidosis. One of the patients had features of rhabdomyolysis as well. The third patient was a substance abuser and had inhaled higher than usual dose and developed severe and refractory acidosis and mild kidney injury and required Renal Replacement Therapy (RRT) for acidosis. All the patients eventually recovered their kidney functions and were doing well during their follow-up.Toluene based organic solvents lead to acute neurological symptoms, accompanied by severe metabolic alterations, organ injury and dysfunc-tion. An association of the development of hypokalemic paralysis and metabolic acidosis with toluene intoxication has been observed. The management of acute toluene toxicity is mainly conservative, consisting of electrolytes correction, acid-base and fluid abnormalities and renal replacement therapy in severe AKI.Organic solvent exposure may result in acute tubular necrosis, rhabdomyolysis, RTA and AKI irrespective of the intake route. Clinical suspicion of organ dysfunction and failure and timely induction of supportive care leads to a good outcome.

Immunoglobulin A nephropathy and IgA vasculitis (HSP)

2020 ◽  
pp. 4909-4917
Author(s):  
Jonathan Barratt ◽  
John Feehally
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Iga Nephropathy ◽  
Systemic Vasculitis ◽  
Treatment Options ◽  
Immunoglobulin A ◽  
Kidney Injury ◽  
Oral Prednisolone ◽  
Immunoglobulin A Nephropathy ◽  
Renal Vasculitis

Immunoglobulin A nephropathy (IgAN) is the commonest pattern of glomerulonephritis identified in areas of the world where renal biopsy is widely practised. It is defined pathologically by IgA deposition in the glomerular mesangium accompanied by a mesangial proliferative glomerulonephritis which may vary greatly in severity. Aetiology is uncertain, but abnormalities of IgA1 hinge-region O-glycosylation are consistently found. Clinical features—IgAN can present with (1) visible haematuria, typically in children and young adults, developing within a day or two of upper respiratory tract infection (‘synpharyngitic’); (2) asymptomatic nonvisible haematuria/proteinuria; (3) nephrotic syndrome (<5% of cases); (4) acute kidney injury (uncommon); and (5) chronic renal failure with up to 25% of patients reaching endstage renal failure within 20 years of diagnosis. Henoch–Schönlein purpura (HSP) is a small vessel systemic vasculitis characterized by small blood vessel deposition of IgA that predominantly affects the skin, joints, gut, and kidney, with nephritis that may be histologically indistinguishable from IgA nephropathy. Management—there is no treatment known to modify mesangial deposition of IgA. Treatment options are mostly directed at controlling blood pressure and limiting proteinuria through blockade of the renin–angiotensin–aldosterone axis. In the rare patient presenting with acute kidney injury in whom biopsy shows crescentic IgA nephropathy, a regimen such as those used for renal vasculitis and other forms of crescentic glomerulonephritis should be considered, for example, oral prednisolone in combination with cyclophosphamide.

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