Long-term CsA therapy in low doses is effective in the treatment of children with idiopathic NS, but the rate of relapse is high after drug withdrawal. Hypertension developed in 10% of patients and renal insufficiency in 6% (most patients with FSGS).

Malaria remains a serious health problem in many parts of the world. It causes high morbidity and claims many lives in developing countries each year. Humans are generally infected by four species of malaria parasites. However, malaria infection caused by Plasmodium malariae or P. falciparum is recognized as an important cause of acute renal failure (ARF) and other renal-related disorders (nephropathy) in infected patients. The increasing incidence of malarial ARF (MARF) and the emergence of clinical malarial infection after renal transplantation represent a serious challenge. Additionally, the impact of immunosuppressive therapies on malarial infection is intricate, complex, and not yet well defined. Pathogenesis of MARF is most likely to be due to immune complex-mediated glomerulonephritis caused by immune-complex deposition and endothelial damage, which may lead to fatal forms of quartan malarial nephropathies. Effects of mechanical, immunologic, cytokine, humoral, acute phase response, and hemodynamics factors in inducing malarial nephropathy have also been postulated. Development of preventive strategies aimed at combating MARF and other renal disorders associated with malaria infection requires (1) prevention of malarial infection, (2) early diagnosis, and (3) early referral to well-equipped centers to provide renal replacement therapy, if necessary, along with antimalarial therapy and support. These measures could significantly reduce mortality and enhance recovery of renal function.

Raised level of Il-6 and TNF-alpha may influence the development of anemia in Egyptian patients with Lupus Nephritis.

Acute kidney injury (AKI) is a complex clinical condition associated with significant morbidity and mortality and lacking effective management. Ischemia-reperfusion injury (IRI) remains one of the leading causes of AKI in native and transplanted kidneys. The aim of this study was to evaluate the efficacy of adipose-derived mesenchymal stem cells (ADSCs) in the prevention of renal IRI in rats. The study was conducted on male Sprague-Dawley rats (n=72) weighing 250–300 g. Rats were randomly assigned to three main groups: i) Sham-operated control group (n=24); ii) positive control group, in which rats were subjected to IRI and were administered culture media following 4 h of IRI (n=24); and iii) ADSC group (n=24), in which rats were administered 1×106 ADSCs via the tail vein following 4 h of IRI. Each main group was further divided according to the timing after IRI into four equal-sized subgroups. Renal function was tested via the measurement of serum creatinine levels and creatinine clearance. In addition, malondialdehyde (MDA) levels were determined in serum and renal tissue homogenate as an indicator of oxidative stress. Histopathological changes were analyzed in different regions of the kidney, namely the cortex, outer stripe of the outer medulla (OSOM), inner stripe of the outer medulla (ISOM) and inner medulla. In each region, the scoring system considered active injury changes, regenerative changes and chronic changes. The ADSCs were assessed and their differentiation capability was verified. IRI resulted in a significant increase in serum creatinine, serum and tissue MDA levels and a significant reduction in creatinine clearance compared with those in sham-operated rats,. These changes were attenuated by the use of ADSCs. The prominent histopathological changes in the cortex, ISOM and OSOM were reflected in the injury score, which was significantly evident in the positive control group. The use of ADSCs was associated with significantly lowered injury scores at days 1 and 3; however, no significant effect was observed on day 7. These results indicate that the use of ADSCs ameliorates renal injury and dysfunction associated with IRI in rats.

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