scholarly journals Cisplatin-Induced Nephrotoxicity and HIV Associated Nephropathy: Mimickers of Myeloma-Like Cast Nephropathy

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Muhammad Siddique Khurram ◽  
Ahmed Alrajjal ◽  
Warda Ibrar ◽  
Jacob Edens ◽  
Umer Sheikh ◽  
...  
Keyword(s):  
Plasma Cell Dyscrasia ◽  
Renal Tubules ◽  
High Electron ◽  
Hiv Patients ◽  
Pneumocystis Jiroveci ◽  
The Third ◽  
Cast Nephropathy ◽  
Myeloma Cast Nephropathy ◽  
Foot Process ◽  
Tubular Dilatation

Myeloma cast nephropathy is an obstructing disorder of renal tubules, caused by precipitation of Bence Jones proteins. Myeloma-like cast nephropathy (MLCN) has been reported in the literature to occur in various primary renal and nonrenal diseases. We present a series of three rare cases of cast nephropathy, two of which are HIV patients, and the third patient is receiving cisplatin-based chemotherapy. However, in all three patients plasma cell dyscrasia has been ruled out. A 30-year-old male was admitted to the hospital with facial cellulitis. The second patient is a 31-year-old male who presented with Pneumocystis jiroveci pneumonia. The third patient was treated with cisplatin-based chemotherapy for carcinoma. First two cases revealed foci of diffuse tubular dilatation containing hyaline casts and interstitial inflammatory infiltrate, in addition to globally sclerotic glomeruli with ultrastructural foot process fusion and mesangium expansion. The third case showed acute tubular injury and cast formation of irregular casts composed of amorphous or granular material of low density admixed with scattered high electron-dense globules. Myeloma-like cast nephropathy and true myeloma cast nephropathy pose similar destructive effects on renal parenchyma. This new pattern of HIV-related nephropathy should be considered in HIV patients with MLCN, once monoclonal gammopathy is ruled out.

Plasmapheresis in myeloma cast nephropathy

2013 ◽  
Vol 79 (01) ◽  
pp. 72-77
Author(s):  
Isabelle Chapdelaine ◽  
François Madore
Keyword(s):  
Cast Nephropathy ◽  
Myeloma Cast Nephropathy

Obstructive Protein Cast Nephropathy in Cynomolgus Monkeys Treated with Small Organic Molecules

2008 ◽  
Vol 45 (6) ◽  
pp. 945-948 ◽  
Author(s):  
R. E. Guzman ◽  
K. Datta ◽  
N. K. Khan
Keyword(s):  
Renal Toxicity ◽  
Obstructive Nephropathy ◽  
Drug Induced ◽  
Cast Material ◽  
Small Organic Molecules ◽  
Cynomolgus Monkeys ◽  
Cast Nephropathy ◽  
Cynomolgus Macaques ◽  
Species Specific ◽  
Tubular Dilatation

We have observed a renal toxicity consistent with an obstructive protein cast nephropathy in cynomolgus macaques but not in other species treated with different therapeutic candidates having a common carboxylic acid moiety, suggesting a species-specific sensitivity. Here, we present renal toxicity findings consistent with a protein cast nephropathy in a 2–week safety study in cynomolgus monkeys. Light microscopic changes consisted of intratubular cast formation, tubular dilatation, interstitial inflammation, and expansion of the medullary interstitium. Tubular cast material was identified as Tamm-Horsfall protein (THP) and, on ultrastructure, crystalloid material was present in vacuoles of tubular epithelium. It is hypothesized that microcrystal formation in the urinary tubular spaces induces aggregation of THP protein and cast formation in monkeys. Drug-induced obstructive nephropathy is not identified as a major problem in humans; thus, the clinical relevance of the above findings in monkeys is not clear.

A case of myeloma cast nephropathy complicated by Fabry disease after withdrawal from dialysis

2020 ◽  
Vol 129 (2) ◽  
pp. S164
Author(s):  
Hiroyuki Yamakawa ◽  
Keika Adachi ◽  
Hirobumi Tokuyama ◽  
Shu Wakino ◽  
Tadayashu Togawa ◽  
...  
Keyword(s):  
Fabry Disease ◽  
Cast Nephropathy ◽  
Myeloma Cast Nephropathy

scholarly journals Morphological and immunohistochemical predictors of renal response to therapy patients with myeloma cast nephropathy and dialysis-dependent acute kidney injury

2020 ◽  
Vol 92 (7) ◽  
pp. 63-69
Author(s):  
I. G. Rekhtina ◽  
E. V. Kazarina ◽  
E. S. Stolyarevich ◽  
A. M. Kovrigina ◽  
V. N. Dvirnyk ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Prognostic Value ◽  
Interstitial Fibrosis ◽  
Kidney Injury ◽  
Response To Therapy ◽  
Tubular Damage ◽  
Renal Response ◽  
Cast Nephropathy ◽  
Myeloma Cast Nephropathy ◽  
E Cadherin

Aim.Reveal morphological and immunohistochemical predictors of reversibility of dialysis-dependent acute kidney injury (AKI) in patients with myeloma cast nephropathy (MCN) based on the study of kidney biopsy. Materials and methods.Renal pathological findings were studied in 36 patients with MCN and dialysis-dependent stage 3 AKI (AKIN, 2012). The study of biopsy samples was performed by a semi-quantitative and quantitative analysis using computer morphometry. The expression of E-cadherin, vimentin and-smooth muscle actin was determined immunohistochemically in the tubular cells and interstitium. Induction therapy for 26 patients was carried out to bortezomib-based programs; in 10 patients other schemes were used. A comparative analysis of morphological changes in nephrobiopathy depending on the renal response was performed in patients with achieved hematologic remission. Results.Improved renal function was observed only in patients with hematologic response to therapy. There were no differences in the number of sclerotic glomeruli, protein casts, the area of inflammatory interstitial infiltration, and the degree of acute tubular damage in patients with and without renal response. In patients with renal response compared with patients without improving renal function, the area of interstitial fibrosis was less (24.9% and 45.9%, respectively;p=0.001), and the area of E-cadherin expression was larger (15.9% and 7.1%, respectively;p=0.006). Interstitial fibrosis of 40% or more and/or the area of expression of E-cadherin less than 10% of the area of tubulo-interstitium have an unfavorable prognostic value in achieving a renal response in MCN. Conclusion.If the interstitial fibrosis area is 40% or more and the expression area of E-cadherin is less than 10%, the probability of the absence of a renal response is 93.3% (OR=24.5) even when a hematological response to induction therapy is achieved. The number of protein casts, the prevalence of acute tubular damage and inflammatory interstitial infiltration have not prognostic value.

scholarly journals SP108A SINGLE CENTRE EXPERIENCE ON HIGH CUT-OFF HAEMODIALYSIS FOR TREATMENT OF MYELOMA CAST NEPHROPATHY

2019 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Zi Chan ◽  
Ka Lok Chan ◽  
Chi Kwan Lam ◽  
Wai Ping Law ◽  
Wai Lun Will Pak ◽  
...  
Keyword(s):  
Single Centre ◽  
Cast Nephropathy ◽  
Myeloma Cast Nephropathy ◽  
Single Centre Experience

All That Glitters Yellow Is Not Gold: Presentation and Pathophysiology of Bile Cast Nephropathy

2017 ◽  
Vol 25 (7) ◽  
pp. 652-658 ◽  
Author(s):  
Mitchell Pitlick ◽  
Prerna Rastogi
Keyword(s):  
Liver Disease ◽  
Kidney Biopsy ◽  
Kidney Injury ◽  
Renal Tubules ◽  
Drug Induced ◽  
Underlying Liver Disease ◽  
Drug Induced Liver Injury ◽  
Tubular Necrosis ◽  
Cast Nephropathy ◽  
Severe Hyperbilirubinemia

Background. Acute kidney injury (AKI) often manifests in patients with liver disease because of a prerenal cause and presents as acute tubular necrosis or hepatorenal syndrome. Distinguishing between these entities is important for prognosis and treatment. Some patients may develop AKI related to their underlying liver disease: for example, membranoproliferative glomerulonephritis or IgA nephropathy. Bile cast nephropathy is an often ignored differential diagnosis of AKI in the setting of obstructive jaundice. It is characterized by the presence of bile casts in renal tubules, which can possibly cause tubular injury through obstructive and direct toxic effects. Thus, AKI in patients with liver disease may have a structural component in addition to a functional one. Methods. In this study, we describe 2 patients with severe hyperbilirubinemia who developed AKI and underwent a kidney biopsy that revealed bile casts in tubular lumens, consistent with bile cast nephropathy. Results. One patient was treated aggressively for alcoholic hepatitis and required hemodialysis for AKI. The second patient was treated conservatively for drug-induced liver injury and did not require dialysis. Both patients saw a reduction in their bilirubin and creatinine toward baseline. Conclusion. Bile cast nephropathy is an important pathological entity that may account for the renal dysfunction in some patients with liver disease. It requires kidney biopsy for diagnosis and may often be overlooked given the scarcity of kidney biopsy in this particular clinical setting. The etiology is multifactorial, and it is often difficult to predict without the aid of a renal biopsy.

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