High cut-off hemodialysis and bortezomib-based therapy to rescue kidneys in myeloma-dependent cast nephropathy.

Myeloma-dependent cast nephropathy (MCN) is a medical emergency where prompt medical intervention is essential to rescue the kidneys from irreversible damage and the patient from lifelong dialysis. Evidence of the benefit of plasma exchange in removing serum free light chains (sFLC) has been controversial [1,2]. According to our recent experience, high cut-off hemodialysis (HCOD) with specially designed dialyzers reduces the level of sFLC concentration within hours and improves renal function in MCN in the long term when combined with effective bortezomib-based chemotherapy.

[Acute renal failure]. / Munuaisten akuutti vajaatoiminta.

Acute renal failure occurs in intensive care units as part of multiple organ injuries as well as in connection with sepsis and other severe diseases. The corresponding mortality rate remains high. High age and blood pressure, vascular diseases and diabetes are its risk factors. Angiotensin convertase inhibitors and angiotensin receptor blockers cause a functional "nephrectomy", especially when combined with anti-inflammatory drugs in situations of fluid deficit. Acute ischemic tubular necrosis is the most common cause. Treatment involves usually correction of hemodynamic abnormalities, fluid and other supportive therapy, elimination of obstructions, and dialysis.

Plasma concentrations of asymmetric-dimethyl-arginine in type 2 diabetes associate with glycemic control and glomerular filtration rate but not with risk factors of vasculopathy.

Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS). Increased plasma levels of ADMA may indicate endothelial dysfunction and increased risk of angiopathy. The relation of ADMA to diabetes, glycemic control, and renal function, especially early diabetic hyperfiltration, remains unknown. We tried to evaluate whether there is an association between ADMA and glycosylated hemoglobin (GHbA(1c)) on the one hand and glomerular filtration rate (GFR) on the other hand in diabetic subjects with normal or slightly increased GFR. We also studied whether plasma ADMA is associated with some risk factors of vasculopathy (hypercholesterolemia and hypertension). The study subjects consisted of 86 patients with type 2 diabetes and 65 control subjects. Plasma ADMA levels were measured by high-pressure liquid chromatography as o-pthalaldehyde (OPA) derivatives and GFR was determined by the plasma clearance of chromium 51-EDTA. The diabetic patients had lower plasma ADMA levels than the nondiabetic control subjects (0.29 +/- 0.15 v 0.34 +/- 0.16 micromol/L, P <.03). In the diabetic subjects, plasma ADMA concentrations were inversely correlated with GHbA(1c) (R = -0.28, P =.01). In a multivariate linear model, significant predictors of ADMA were GFR (R = -0.32, P =.008) in diabetic subjects and GHbA(1c) (R = -0.19, P =.03) and GFR (R = -0.19, P =.02) in all subjects. Plasma ADMA was not associated with risk factors of vasculopathy. We conclude that diabetic patients with a normal or slightly increased GFR have lower circulating ADMA concentrations than nondiabetic control subjects. In type 2 diabetic patients high GFR and poor glycemic control were related to low plasma ADMA concentrations.

Incidence of biopsy-proven glomerulonephritis.

BACKGROUND: The reported biopsy-proven glomerulonephritis incidence varies according to population characteristics, the unknown true glomerulonephritis incidence and biopsy rate. Reported glomerulonephritis incidence should be evaluated against the biopsy rate. METHODS: We report here the glomerulonephritis incidence in our University Hospital (UH) consecutive biopsy material. It is compared to those from surrounding central hospitals (CH), previous single-centre studies and European biopsy registries (EBR). Biopsy rate, when reported, has been considered. RESULTS: The annual biopsy rate/10(5), median (min-max), at the UHs was 25.4 (15.6-35.1). At the CHs it was 8.7 (5.1-12.6). In previous single-centre studies it has been 18.7-21.5. In the EBRs it has been between 1.0 and 6.9 when reported. The annual incidences (median, min-max) per 10(5) (1980-2000) at the UH were as follows: proliferative glomerulonephritis (9.5, 6.8-18.1), non-proliferative glomerulonephritis (6.7, 3.4-12.6), the four major glomerulonephritis groups MesGN (7.7, 4.4-15.9), ECGN/FPGN-complex (1.4, 0.5-3.2), MCGP/FSGS-complex (0.9, 0.2-2.7) and MGN (1.4, 0.5-2.4) these which findings were compatible with the single-centre studies and higher than those of the CHs and in the EBRs. Biopsy rate had a major impact on the annual glomerulonephritis incidences explaining 60% of the variation. The relative frequency of MesGN was the highest by all observers, followed by the ECGN/FPGN-complex, MGN and MCGP/FSGS-complex whose frequencies did not differ much. For every patient commencing renal replacement therapy (Finnish Renal Replacement Registry Data) due to glomerulonephritis there were about 11 subjects with biopsy-proven glomerulonephritis, a relationship compatible with previous reports. CONCLUSIONS: The incidence of any glomerulonephritis of 17.6 per 10(5) population was comparable to those from the single-centre studies, but higher than in European biopsy registries, a fact largely explained by biopsy rates.

Thalidomide in POEMS syndrome: case report.

We report a patient with incapacitating POEMS syndrome characterized by serum monoclonal protein, polyneuropathy, organomegaly, endocrinopathy, mesangiocapillary glomerulonephritis, massive ascites formation, and pulmonary hypertension. A dramatic improvement in the clinical condition occurred after administration of thalidomide, a drug with known anti-angiogenetic, anti-proliferative, and anti-cytokine properties.

Apolipoprotein E gene polymorphism, hypercholesterolemia and glomerular filtration rate in type 2 diabetic subjects: a 9-year follow-up study.

OBJECTIVE: To study the association between apolipoprotein E (apoE) genotype and the rate of decline in glomerular filtration rate (GFR) in type 2 diabetic patients in a 9-year prospective study. METHODS: GFR was determined in 84 type 2 diabetic patients by plasma clearance of (51)Cr-EDTA at baseline and after 9 years of follow-up. ApoE genotypes were determined by polymerase chain reaction and restriction enzyme HHAI digestion and designated as epsilon4 allele group (apoE4/2, 4/3 and 4/4 genotypes; n = 20) and non-epsilon4 allele group (apoE3/3 and E3/2 genotypes; n = 64). We focused our analysis on those patients who were more likely to progress to diabetic renal disease, i.e. whose GFR fell more than expected in the normal course of ageing [1 ml x min(-1) x (1.73 m(2))(-1) per year]. RESULTS: In the whole population, the decline in the GFR did not differ statistically significantly between the apoE genotype groups [p = 0.65 with analysis of variance for repeated variables (RANOVA) for interaction between apoE genotype group and time point]. However, among patients whose GFR changed more than 9 ml x min(-1) x (1.73 m(2))(-1), GFR showed a statistically significantly greater decline in the epsilon4 allele group (n = 11) than in the non-epsilon4 allele group (n = 43) [from 116 +/- 36 to 80 +/- 29 ml x min(-1) x (1.73 m(2))(-1) vs. from 119 +/- 20 to 96 +/- 18 ml x min(-1) x (1.73 m(2))(-1); p = 0.005 with RANOVA]. CONCLUSION: ApoE allele epsilon4 may speed up the rate of decline of the GFR in patients with progressive diabetic renal disease.