Prevalence of systemic co-morbidities in patients with various grades of diabetic retinopathy.

Background & objectives: Though diabetes affects multiple organs, most studies highlight the occurence of only one complication in isolation. We conducted a hospital-based study to estimate the co-existence of significant systemic co-morbid conditions in patients with varying grades of diabetic retinopathy. Methods: A total of 170 consecutive patients with diabetic retinopathy were prospectively recruited for the study between June 2009 to June 2010 at a tertiary care eye centre in north India. Retinopathy was graded by fundus biomicroscopy and fundus photography and classified into three categories (mild-moderate nonproliferative retinopathy, proliferative retinopathy requiring only laser and proliferative retinopathy requiring surgery). Nephropathy was classified by calculating the six variable estimated glomerular filtration rate (eGFR) for all patients. Nerve conduction studies and clinical assessment were used to determine presence of neuropathy. Co-existence of macrovascular disease and peripheral vascular disease was also ascertained. Results: The percentages of patients with overt nephropathy in the three groups were 19.2, 38.0 and 41.2, respectively. Significant linear trends were observed for serum creatinine (P=0.004), albumin (P=0.017) and eGFR (P=0.030). A higher per cent had abnormal nerve conduction on electrophysiology than that diagnosed clinically (65.4 vs. 44.2, 76.0 vs. 40.0 and 64.8 vs. 48.6, respectively). The odds ratio (95% CI) for co-existence of nephropathy, neuropathy, CVA (cerebrovascular accidents) and PVD (peripheral vascular disease) was 2.9, 0.9, 4.8 and 3.5, respectively. Independent of retinopathy severity, patients with clinically significant macular oedema (CSME) had a higher percentage of nephropathy (pP < 0.005). Interpretation & conclusions: The co-existence of overt nephropathy, nerve conduction based neuropathy and macrovascular co-morbidity in patients with early grades of diabetic retinopathy was significant. Screening for overt nephropathy by eGFR should be considered in all patients with clinically significant macular oedema.

Bone marrow cells contribute to tubular epithelium regeneration following acute kidney injury induced by mercuric chloride.

Background & objectives: Acute tubular necrosis (ATN) caused by renal ischaemia, renal hypo-perfusion, or nephrotoxic substances is the most common form of acute kidney injury (AKI). There are a few treatment options for this life-threatening disease and the mortality rate exceeds 50 per cent. In critical cases of AKI the only option is renal transplantation. In the present study we evaluated whether bone marrow cells (BMCs) are involved in regeneration of kidney tubules following acute tubular necrosis in the mouse. Methods: Six to eight week old C57BL6/J and congenic enhanced green fluorescence protein (eGFP) mice were used. The relative contributions of eGFP-expressing BMCs were compared in two different approaches to kidney regeneration in the mercuric chloride (HgCl2)-induced mouse model of AKI: induced engraftment and forced engraftment. In vitro differentiation of lineage-depleted (Lin-) BMCs into renal epithelial cells was also studied. Results: In the forced engraftment approach, BMCs were found to play a role in the regeneration of tubules of renal cortex and outer medulla regions. About 70 per cent of donor-derived cells expressed megalin. In vitro culture revealed that Lin- BMCs differentiated into megalin, E-cadherin and cytokeratin-19 (CK-19) expressing renal epithelial cells. Interpretation & conclusions: The present results demonstrate that Lin- BMCs may contribute in the regeneration of renal tubular epithelium of HgCl2-induced AKI. This study may also suggest a potential role of BMCs in treating AKI.

IgM nephropathy in adults: incidence and correlation with electron microscopic features.

IgM nephropathy is characterised on light microscopy (LM) by variable features of normal glomeruli to mesangial hypercellularity; and immunofluorescence (IF) deposits of LgM. Our aim was to study the incidence of IgM nephropathy in adults with primary glomerular disease, with correlation to electron microscopy (EM) features. All adults presenting with proteinuria glomerular hematuria underwent renal biopsy. We excluded patients with systemic diseases and post-infectious glomerulonephritis. All the specimens were evaluated by LM, IF and EM. Our series had 146 cases. Of the 42 cases diagnosed on LM as minimal change disease, mesangial deposition of IgM was present in 11 cases. In addition there were seven cases of mesangioproliferative glomerulonephritis with mesangial IgM deposition. Thus, there were a total of 18 cases of IgM nephropathy (12.3%). Only six of these 18 cases showed typical electron dense deposits in the mesangium on EM. We feel that IgM nephropathy is probably a separate pathological entity, comprising 12.3% of all adults with primary chronic glomerulopathy. Electron dense deposits are seen in only about a third of these cases.

Multiple myeloma presenting as collapsing glomerulopathy.

A 54 year old male patient was admitted with advanced renal failure of recent onset. Serology was noncontributory. Renal biopsy showed collapsing glomerulopathy with interstitial fibrosis. Bone marrow examination confirmed the diagnosis of multiple myeloma. With chemotherapy multiple myeloma went into remission. However he continued to remain dialysis dependent and a repeat kidney biopsy showed progression to endstage renal disease.