Diabetic nephropathy is a major cause of end-stage renal failure and the mortality rate due to this disease is continuously progressing worldwide. The multifaceted signalling mechanisms have been identified to be involved in the pathogenesis of diabetic nephropathy. Despite the modern therapies like antidiabetics, antihypertensives, and antioxidants available to treat diabetic nephropathy; most of patients continue to show progressive renal damage. It suggests that the key pathogenic mechanism involved in the induction and progression of diabetic nephropathy is still remaining active and unmodified by the present therapies. The purpose of this review is to bring together the current information concerning the signalling systems involved in the pathogenesis of diabetic nephropathy.

Nephropathy is a leading cause of morbidity and mortality and its prevalence is continuously increasing in industrialised nations. Nephropathy is characterised to varying degrees by nodular glomerulosclerosis, glomerular basement membrane thickness and mesangial expansion, leading to a decline in glomerular filtration rate, persistent elevated albuminuria, elevated arterial blood pressure and fluid retention. Hyperglycaemia, hyperlipidaemia and hypertension are considered to be the major risk factors implicated in the progression of nephropathy. Various signalling systems, such as vasoconstrictor peptides, inflammatory mediators, growth factors and adhesion molecules, are involved in the pathogenesis of nephropathy. At present, no promising therapy is available to treat patients with nephropathy due to lack of understanding of signalling culprits involved in the pathogenesis of nephropathy. Animal models are being developed to better understand the disease pathogenesis and develop drugs for nephropathy. In the present review, we have discussed various animal models for nephropathy, which may open vistas for developing new drugs to treat nephropathy.

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Diabetic nephropathy is associated with high morbidity and mortality and the prevalence of this disease is continuously increasing world wide. Though, the major risk factors like hyperglycemia and hypertension play a pivotal role in the pathogenesis of diabetic nephropathy, the etiology of this insidious disorder is not well understood. Mast cells are pluripotent bone marrow derived cells that play a key role in inflammation. Degranulation of mast cells releases various mediators including inflammatory cytokines, endothelins, growth factors, and proteolytic enzymes. Infiltration of mast cells has been noted to occur in renal diseases. In addition, the renal density of mast cells is significantly increased in diabetic patients with nephropathy. It remains unclear whether resident renal mast cells derived mediators play a role in the pathogenesis of diabetic nephropathy. Recent studies suggest the involvement of renal mast cell infiltration and degranulation in diabetic nephropathy. The present review focuses on the role of resident renal mast cells in diabetic nephropathy.

Snake bite is a common clinical problem in Southern Africa. In spite of this, acute renal failure from snake-bite poisoning is extremely rare. Moreover, acute renal failure from puff adder (Bitis arietans) has to our knowledge not been described previously. Two cases of acute renal failure occurring after puff adder venom poisoning were seen within a period of 6 weeks and are described here. Both these patients were maintained on haemodialysis and recovery was uneventful. In both cases, a proliferative nephritis was seen on renal biopsy. It is postulated that the snake venom produced the proliferative nephritis on a hypersensitivity basis.