Membranoproliferative glomerulonephritis: A rare presentation of occult filariasis

Parasitic infections do not usually present with rapidly progressive renal failure but can provoke glomerular lesions which are mostly proliferative. In filarial infection, glomerular involvement is usually mild and transient, and presentation with renal failure is rare. We report occult filariasis presenting as rapidly progressive renal failure due to immune-complex mediated membranoproliferative glomerulonephritis. Our patient responded to treatment with diethylcarbamazine and a short course of steroid. This case highlights the importance of thorough workup to identify the cause and consideration of filariasis in an endemic area.

MO101ASSESSING EARLY RENAL INVOLVEMENT IN ESSENTIAL HYPERTENSION BY MEASURING URINARY ALBUMIN AND UROMODULIN EXCRETION

Background and Aims Kidneys are target organs in hypertension. Hypertensive damage results in glomerular as well as tubular dysfunction. Albuminuria is a known marker of glomerular damage. Whereas, urinary uromodulin is increasingly considered as potential biomarker of early tubular dysfunction. The aim of this study was to identify the pattern of early renal involvement based on glomerular and tubular function assessment by measuring urinary albumin and uromodulin in hypertensive patients Method In this cross-sectional study 122 hypertensive subjects with age>30 years, duration of hypertension <5years, without accelerated or malignant BP, absence of dipstick proteinuria and eGFR>60ml/min. Subjects with possibility of secondary hypertension were excluded. There were also 33 normotensive volunteers included as healthy referents. Morning spot urine for albumin-creatinine ratio (ACR mg/g), urine uromodulin-creatinine ratio (urUMODµg/g), urinary sodium-creatinine ratio (mEq/g) and potassium-creatinine ratio (mEq/g) were measured in single urine sample. Urine uromodulin was measured by ELISA method. Results The hypertensive and healthy subjects were matched for age 48±11 vs. 47±11, years (P=NS). The systolic BP was 145±15 vs. 112±12 mmHg and diastolic BP 86±9 vs. 70±8 mmHg; (p<0.001) and the mean ACR was 29±65 vs. 5.6±2.7 mg/g, (p<0.001) respectively. Around 20% hypertensives had albuminuria. Urinary potassium excretion was lower in hypertensives (51±31 vs. 69±31, mEq/g; p<0.02). The median urUMOD in hypertensive subjects was 3.38 (1.73-9.06) and in normotensives 3.85(2.28-5.69) µg/g (P=NS).Multivariate analysis showed significant inverse association between diastolic blood pressure and urinary uromodulin excretion. An urURMOD cut-off of 2.9 (25th percentile in normotensives) showed eGFR, urinary sodium & potassium excretions were significantly lower at low uromodulin cut-off and this was seen in38%subjects. Conclusion The glomerular involvement was found in 20% hypertensives as evidenced by albuminuria. In general urinary uromodulin level was not different between hypertensive and normotensive subjects. Association of low uromodulin cut-off with lower eGFR, Na+ and K+ excretion indicates simultaneous tubule glomerular involvement in 38%.

Glomerular podocyte dysfunction in inherited renal tubular disease

Background Hereditary renal tubular disease can cause hypercalciuria, acid-base imbalance, hypokalemia, hypomagnesemia, rickets, kidney stones, etc. If these diseases are not diagnosed or treated in time, they can cause kidney damage and electrolyte disturbances, which can be detrimental to the maturation and development of the child. Glomerular involvement in renal tubular disease patients has only been considered recently. Methods We screened 71 papers (including experimental research, clinical research, etc.) about Dent’s disease, Gitelman syndrome, and cystinosis from PubMed, and made reference. Results Glomerular disease was initially underestimated among the clinical signs of renal tubular disease or was treated merely as a consequence of the tubular damage. Renal tubular diseases affect glomerular podocytes through certain mechanisms resulting in functional damage, morphological changes, and glomerular lesions. Conclusions This article focuses on the progress of changes in glomerular podocyte function in Dent disease, Gitelman syndrome, and cystinosis for the purposes of facilitating clinically accurate diagnosis and scientific treatment and improving prognosis.

Case report: a man with untreated rheumatoid arthritis, cryoglobulinemic vasculitis, membranous nephropathy and pulmonary sarcoidosis

Background Glomerular involvement in rheumatoid arthritis has been known to be associated with treatment side effects from medications and secondary amyloidosis. However, limited basic science and clinical studies have been performed to address the potential disease specific immune-mediated mechanisms causing secondary glomerular pathology, its various types of presentation, and the potential treatments. Case presentation A 41-year-old man with chronic active rheumatoid arthritis presented with nephrotic syndrome and was found to have membranous nephropathy with eosinophilic intracapillary thrombi on renal biopsy. Proteinuria persisted despite complete withdrawal from non-steroidal anti-inflammatory drugs (NSAIDs) and disease-modifying anti-rheumatic drugs (DMARDs). Throughout the disease course, he developed cryoglobulinemic vasculitis and pulmonary sarcoidosis, both of which achieved clinical resolution with glucocorticoids. However, only partial improvement was observed in proteinuria with treatment of steroids and Rituximab. Conclusion Our case presented a unique and complicated clinical phenotype of active rheumatoid arthritis, with clinical features of cryoglobulinemic vasculitis, histopathologic features of membranous and cryoglobulinemic nephropathy in the absence of DMARDs use, as well as pulmonary sarcoidosis. We speculate that there is a wider spectrum of glomerular disease in patients with untreated rheumatoid arthritis. In addition, the potential association between rheumatoid arthritis and cryoglobulinemic vasculitis should probably be revisited and requires further studies to elucidate the underlying mechanisms and treatment options.

First Case of COVID-19-Associated Collapsing Glomerulopathy in Sub-Saharan Africa

Although the lungs remain the main target of SARS-CoV-2, other organs, such as kidneys, can be affected, which has a negative impact on the outcomes of COVID-19 patients. Although previous studies of kidney disease in COVID-19 reported mainly SARS-CoV-2-induced tubular and interstitial injury, there is growing evidence coming out of Africa of glomerular involvement, especially collapsing glomerulopathy seen particularly in people of African descent. We report a case of collapsing glomerulopathy revealed by acute kidney injury and a new onset of full blown nephrotic syndrome in a black Congolese patient coinfected with COVID-19 and malaria.