The kidneys are affected in almost all patients with amyloid A in secondary amyloidosis (AA) amyloidosis but less frequently in immunoglobulin light chains in primary systemic amyloidosis (AL) amyloidosis. In this study, we present the incidence, etiology, clinical manifestations, biochemical features and clinical course of renal amyloidosis. We conducted a retrospective study on a group of 40 cases with renal biopsy-proven amyloidosis. They constituted 2.5% of the total cases of renal biopsies performed in the Theodor Bilharz Research Institute, Cairo, Egypt, during the period from February 2003 to May 2009. The mean age (30 males, ten females) was 36.51 ± 10.32 years. Thirty-two of the cases had secondary AA amyloidosis and eight cases had primary AL amyloidosis. The causes of secondary amyloidosis were as follows: 12 (30%) familial Mediterranean fever (FMF), eight (20%) pulmonary tuberculosis, four (10%) chronic osteomyelitis, four (10%) bronchiectasis, three (7%) rheumatoid arthritis and one (2%) rheumatic heart disease. The eight cases of primary AL amyloidosis comprised of five cases that were associated with myloma (13%) and three (8%) cases that were idiopathic. Among the 23 patients with AA amyloidosis, after six months of treatment with colchicine, the proteinuria improved, serum albumin level increased and edema disappeared in 13 patients. In four cases of AA amyloidosis who were clinically and biochemically normal after cholchicine therapy, a second renal biopsy disclosed decreased amyloid deposition compared with the first biopsy. In the three renal transplanted patients who had amyloidosis secondary to FMF and were treated with colchicines, AA amyloidosis did not recur in the transplanted kidney. It might be possible that in AL amyloidosis, treatment with methotrexate, melphalan and prednisolone may improve survival. The incidence of renal amyloidosis is increasing and colchicine can be used in secondary amyloidosis as it may have an effect on reducing the production of the amyloid precursor proteins and in reducing proteinuria.

Acute kidney injury (AKI) is a common and serious condition in both the inpatient and outpatient settings, and its diagnosis depends on serum creatinine measurements. Unfortunately, creatinine is a delayed and unreliable indicator of AKI. The lack of early biomarkers has limited our ability to translate promising experimental therapies to human AKI. Fortunately, understanding the early stress response of the kidney to acute injuries has realized a number of potential biomarkers. For example, neutrophil gelatinase-associated lipocalin is emerging as an excellent stand alone troponin-like biomarker in the plasma and urine for predicting and monitoring clinical trials and in the prognosis of AKI. In recent years, a number of new biomarkers of AKI with more favorable test characteristics than creatinine have been identified and studied in a variety of experimental and clinical settings. This review will consider the most well-established biomarkers of AKI.

Background: Adiponectin (ADPN) levels are consistently elevated among patients with advanced chronic kidney disease, but its relationship with cardiovascular outcomes in this population remains controversial. The aim of our study was to measure the plasma levels of ADPN in patients with end-stage renal disease on maintenance hemodialysis (HD) and we studied its correlates to cardiovascular outcomes and mortality. Methods: Our study included 133 HD patients (79 male and 54 female patients) with a mean age of 54.6 ± 17.3 years who had been receiving regular HD for at least 6 months in the nephrology units of Theodor Bilharz Research Institute, Cairo, Egypt. The clinical and biochemical correlates of plasma ADPN levels were investigated and the predictive power of ADPN levels with respect to cardiovascular events and mortality was prospectively tested in HD patients, who were monitored for 24 ± 9 months. Plasma ADPN levels were measured by using a sensitive enzyme-linked immunosorbent assay. Results: Plasma ADPN levels were 3 times higher (p < 0.0001) among HD patients (18.1 ± 6.8 µg/ml) than among healthy subjects (6.2 ± 1.8 µg/ml). Plasma ADPN levels were lower (p < 0.007) among patients who experienced new cardiovascular events (13.9 ± 6.4 µg/ml) than among event-free patients (18.6 ± 8.4 µg/ml). The relative risk of cardiovascular events was 1.96 times (95% confidence interval 1.290–2.977, p = 0.0016) higher among patients in group 1 (ADPN <15.1 µg/ml), compared with those in group 2 (ADPN ≥15.1 µg/ml). Plasma ADPN levels were inversely related to BMI, insulin levels, homeostatic model assessment index values, triglyceride and LDL-C, CRP and left ventricular mass index. Furthermore, plasma ADPN levels were directly related to HDL-C. Conclusion: Plasma ADPN is an independent (inverse) predictor of cardiovascular events and mortality among HD patients. The directions of the relationships between ADPN and several metabolic risk factors indicate that ADPN has a protective role in prevention of CVD.

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BackgroundInterleukin-10 (IL-10) is an important immunoregulatory cytokine. There are few studies evaluating the association between IL-10 and lupus nephritis (LN). The aim of this study was to evaluate the association of IL-10 gene promoter -592 A/C with LN susceptibility.MethodsThe study was conducted on 84 patients with systemic lupus erythematosus (SLE). Patients were divided into LN group (Group I, 48 patients) and non-LN group (Group II, 36 patients). The -592 A/C polymorphisms in IL-10 promoter gene were determined by polymerase chain reaction and restriction fragment length polymorphism in both groups. IL-10 was determined by enzyme-linked immunosorbent assay. Frequencies of the genotypes were compared between LN and non-LN patients and among LN patients with different pathologic classes.ResultsThere was a significant increase in serum level of IL-10 (P = 0.001) in Group I compared with Group II and significant positive correlation between serum IL-10 and SLE disease activity index (r = 0.466, P = 0.001) in Group I. There were no significant differences in the distribution of the IL-10 gene promoter -592 A/C genotypes or the allele frequencies between Groups I and II. There was no significant difference between AC/CC and AA genotypes with SLE disease activity index, proteinuria, hematuria, anti-double-stranded DNA, and IL-10 in Group I. There was no significant difference in the distribution of AC and CC genotypes among different pathologic LN classes.ConclusionIL-10 suggested to play a role in pathogenesis and development of LN. However, the promoter -592 A/C of IL-10 gene suggested to be not associated with serum IL-10 levels or LN susceptibility. In addition, it appears that promoter -592 A/C of IL-10 gene not associated with LN activity or the pathologic classes of LN.

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