scholarly journals Type II Cryoglobulinaemia causing Monoclonal Gammopathy of Renal Significance

2021 ◽  
Vol 20 (3) ◽  
pp. 227-230
Author(s):  
B Mohidin ◽  
◽  
M Sheaff ◽  
RD Wheeler ◽  
G Khamba ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Renal Function ◽  
Renal Impairment ◽  
Acute Ischaemic Stroke ◽  
Membranoproliferative Glomerulonephritis ◽  
Monoclonal Gammopathy ◽  
Microscopic Haematuria ◽  
Type Ii ◽  
Blood Tests ◽  
Nephrotic Range Proteinuria

A 53 year old female with a background of hypertension, hypothyroidism and Raynaud’s was admitted with an acute ischaemic stroke and referred to the renal team after a routine urine dip revealed microscopic haematuria and nephrotic-range proteinuria. Blood tests revealed renal impairment, a monoclonal IgM kappa paraprotein, low complement C4 concentration and a positive rheumatoid factor. Active cryoglobulinaemia was suspected and testing demonstrated type II cryoglobulins secondary to the monoclonal IgM kappa paraprotein. Bone marrow biopsy was normal. Renal biopsy revealed cryoglobulinaemia associated membranoproliferative glomerulonephritis. Treatment with steroids and rituximab improved renal function and proteinuria. This case fits within the evolving spectrum of disorders now termed Monoclonal Gammopathy of Renal Significance and highlights the value of biopsying and treating these patients early.

Secondary monoclonal gammopathy after bone marrow autotransplantation as a cause of worse renal function in light chain immunoglobulin deposition disease

2016 ◽  
Vol 88 (6) ◽  
pp. 80
Author(s):  
I. G. Rekhtina ◽  
L. P. Mendeleeva ◽  
E. S. Stolyarevich ◽  
I. V. Galtseva ◽  
P. E. Povilaitite ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Renal Function ◽  
Light Chain ◽  
Monoclonal Gammopathy ◽  
Deposition Disease ◽  
Light Chain Immunoglobulin

scholarly journals Progression of Monoclonal Gammopathy with Undetermined Significance to Multiple Myeloma Diagnosed by Kidney Biopsy: A Case Report

2015 ◽  
Vol 5 (3) ◽  
pp. 180-186 ◽  
Author(s):  
Jin Hae Kim ◽  
Ji Won Kim ◽  
Young Nam Kim ◽  
Hye In Kim ◽  
Jun Young Kim ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Renal Function ◽  
Case Report ◽  
Monoclonal Gammopathy ◽  
Kidney Biopsy ◽  
M Protein ◽  
Tubular Proteinuria ◽  
Risk Of Progression ◽  
Undetermined Significance

Monoclonal gammopathy with undetermined significance (MGUS) carries a risk of progression to multiple myeloma, and progression is usually diagnosed with changes in M-protein or bone marrow biopsy. We report a case of 62-year-old female patient showing MGUS progression to multiple myeloma without significant changes in M-protein but diagnosed by kidney biopsy. During the follow-ups, azotemia and tubular proteinuria were aggravated without elevation of M-protein. Kidney biopsy showed intratubular and glomerular inclusions associated with plasma cell dysplasia. The progression of MGUS to multiple myeloma was diagnosed by this kidney biopsy. The patient's renal function and tubular proteinuria were markedly improved after chemotherapy.

Serum Free Light Chains Identify Patients With Monoclonal Gammopathy At Increased Risk Of Developing Renal Disease

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1876-1876 ◽  
Author(s):  
Lawrence R. Johnson ◽  
Gerald C. Miller ◽  
Spencer R. Stout
Keyword(s):  
Renal Function ◽  
Kidney Disease ◽  
Renal Impairment ◽  
Renal Disease ◽  
Kidney Function ◽  
Monoclonal Gammopathy ◽  
Normal Kidney ◽  
Serum Free ◽  
Increased Risk

Abstract Background Monoclonal gammopathy (MG) is frequently associated with kidney disease (monoclonal gammopathy of renal significance; MGRS). International guidelines recommend the use of the serum free light chain (FLC) assay when screening for monoclonal gammopathies; an abnormal FLC ratio and an elevation of at least one FLC isotype indicates an Ig LC clone. However it is not known if, in patients with normal kidney function, the presence of a FLC clone predisposes to the future development of kidney disease. Patients and Methods A 22485 patient database with multiple laboratory tests and up to 15-year follow up (Regional Medical Laboratory, Tulsa, OK, USA) was analysed. There were 425 confirmed MG patients with no progression to multiple myeloma. Median age was 72 years (22-97 years) and M/F ratio was 177/248. FLC kappa and lambda were measured nephelometrically with Freelite® (The Binding Site Ltd, Birmingham, UK). Baseline was defined on the first available FLC measurement; this was available at inception in 258 (61%) patients and during follow-up in 167 (39%) patients. 128 patients with MG and an eGFR <60ml/min/1.75m2 and/or a clinical diagnosis of renal disease (ICD9 code) prior to and up to 100 days after baseline were excluded from the analysis. Statistical analyses, including Receiver Operating Characteristics (ROC) to identify monoclonal FLC (iFLC) cut-off were carried out using SPSS v21. Results 297 (of 425) patients had a MG with normal renal function at baseline; 118 (40%) patients had an abnormal FLC ratio (88 kappa, median: 35.5 (7.7-2675) mg/L; 30 lambda, median: 83.6 (0.9-3552) mg/L). 21/297 (7%) patients developed renal impairment during the course of follow up (median: 852 (114-2388) days); 15/21 (71%) had monoclonal FLC production. In these patients there was no association between iFLC (median: 47.8 (0.9-3552) mg/L) and creatinine (median: 0.9 (0.5-1.5) mg/dL) levels (p=0.3966). Time to renal impairment (TTRI) was significantly shorter for patients with an abnormal v normal FLC ratio (75% TTRI: 1261 days v not reached (NR), hazard ratio (HR): 5.31; p<0.001). Age between groups was similar (median: 68 (22-97) v 72 (39-92) years; p=0.0544). In 118 patients withan abnormal FLC ratio, Cox regression analysis identified iFLC concentrations as being associated with the development of impaired renal function (p=0001). Furthermore, patients with iFLC>100mg/L (n=25) were at a significantly increased risk of developing renal impairment compared with patients with iFLC<100mg/L (n=93) (75% TTRI: 874 days v NR, respectively; HR: 6.10; p<0.001). Conclusions These results indicate that the presence of an Ig LC clone is associated with an increased risk of people with MG and normal kidney function progressing to renal disease. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Efficacy and safety of urate-lowering therapy in people with kidney impairment: a GCAN-initiated literature review

2021 ◽  
Author(s):  
Hamish Farquhar ◽  
Ana B Vargas-Santos ◽  
Huai Leng Pisaniello ◽  
Mark Fisher ◽  
Catherine Hill ◽  
...  
Keyword(s):  
Renal Function ◽  
Renal Impairment ◽  
Case Reports ◽  
Serum Urate ◽  
Cochrane Library ◽  
Future Studies ◽  
Kidney Impairment ◽  
The Cochrane Library ◽  
Study Designs ◽  
Different Levels

Abstract Objectives To evaluate the efficacy, defined as achieving target serum urate &lt;6.0 mg/dl, and safety of urate-lowering therapies (ULT) for people with gout and CKD stages 3–5. Methods PubMed, The Cochrane Library, and EMBASE, were searched from 1 January 1959 to 31 January 2018 for studies that enrolled people with gout, who had an estimated glomerular filtration rate (eGFR) or creatinine clearance (CrCl) of &lt; 60 mL/min, and exposure to allopurinol, febuxostat, probenecid, benzbromarone, lesinurad or pegloticase. All study designs other than case reports were included, except for people on dialysis, for which we did include case reports. Results There were 36 reports with an analysis of efficacy and/or safety based upon renal function – allopurinol (n = 12), febuxostat (n = 10), probenecid (n = 3), benzbromarone (n = 5), lesinurad (n = 5), and pegloticase (n = 1). There were 108 reports that involved people with gout and renal impairment but did not contain any analysis on efficacy and/or safety based upon renal function – allopurinol (n = 84), febuxostat (n = 14), benzbromarone (n = 1), lesinurad (n = 3), and pegloticase (n = 6). Most studies excluded people with more severe degrees of renal impairment (eGFR or CrCl of &lt; 30mL/min). For allopurinol in particular, there was significant variability in the dose of drug used, and efficacy in terms of urate lowering, across all levels of renal impairment. Conclusion There is a lack of evidence regarding efficacy and/or safety of currently used ULT according to different levels of renal function. Future studies should include patients with CKD and should report study outcomes stratified by renal function.

P0234LOW URINARY CITRATE LEVELS ARE NOT SPECIFIC OF AUTOSOMAL POLYCYSTIC KIDNEY DISEASE (ADPKD) AND ARE PRESENT WHEN RENAL FUNCTION IS IMPAIRED IN ALL NEPHROPATIES

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Francisco-Jose Borrego-Utiel ◽  
Enoc Merino Garcia ◽  
Isidoro Herrera ◽  
Clara Moriana Dominguez ◽  
Victoria Camacho Reina ◽  
...  
Keyword(s):  
Renal Function ◽  
Uric Acid ◽  
Kidney Disease ◽  
Renal Impairment ◽  
Polycystic Kidney Disease ◽  
Normal Renal Function ◽  
Serum Bicarbonate ◽  
Polycystic Kidney ◽  
Glomerular Diseases ◽  
Urinary Citrate

Abstract Background and Aims In polycystic kidney disease (PKD) it is frequently found a reduction in urinary citrate that is related with degree of renal impairment but it is unknown if this alteration is specific or if it is also present in other nephropathies. Recently it has been suggested that urinary citrate could be a marker of covert metabolic acidosis and reflects acid retention in chronic kidney disease (CKD). Our aim was to compare urinary citrate in PKD with other renal diseases and to show its relation with serum bicarbonate and excretion of uric acid and calcium. Method We determined citrate, calcium and uric acid in 24-hour urine in patients with PKD and with other nephropathies with varied degree of renal impairment followed in a outpatient clinic of nephrology. Results We included 291 patients, 119 with glomerular diseases, 116 with PKD, 21 with other nephropathies, and 35 patients with normal renal function. Urinary citrate was higher in women (Females 309±251 mg/gCr vs. males 181±145 mg/gCr, p&lt;0.001) and in patients with normal renal function (normal 380±210 mg/gCr; PKD 203±166 mg/gCr; glomerular 279±282 mg/gCr; p&lt;0,001). PKD patients showed similar values of urinary citrate to patients with glomerular diseases and with other nephropathies. We observed a progressive reduction in urinary citrate parallel to degree of renal impairment, in a comparable way among patients with PKD and glomerular diseases. We did not observe a relationship between urinary citrate and serum bicarbonate levels. Calcium and uric acid elimination in ADPKD patients was similar to other nephropathies and lower to patients with normal renal function. However, serum uric acid was significantly higher in glomerular patients than other nephropathies after adjust with glomerular filtration rate and sex. Conclusion Hypocitraturia is not specific of PKD but it is also present in all nephropathies. Urinary citrate are related to degree of renal impairment and it is not related with serum bicarbonate. We think that it could be interesting to study urinary citrate as a marker of renal function and its role as prognostic factor of renal deterioration.

scholarly journals Membranoproliferative Glomerulonephritis Type II (Dense Deposit Disease): An Update

2005 ◽  
Vol 16 (5) ◽  
pp. 1392-1403 ◽  
Author(s):  
Gerald B. Appel ◽  
H. Terence Cook ◽  
Gregory Hageman ◽  
J. Charles Jennette ◽  
Michael Kashgarian ◽  
...  
Keyword(s):  
Membranoproliferative Glomerulonephritis ◽  
Dense Deposit Disease ◽  
Type Ii ◽  
Dense Deposit
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