The antiproteinuric effects of ACE inhibitors and lowering blood pressure are greater in patients with a higher baseline urine protein excretion. The greater beneficial effect of ACE inhibitors on renal disease progression in patients with higher baseline proteinuria can be explained by their greater antiproteinuric effects in these patients. The current level of urine protein excretion is a modifiable risk factor for the progression of non-diabetic renal disease. ACE inhibitors provide greater beneficial effect at all levels of current urine protein excretion.

The onset of renal damage in diabetes mellitus may be influenced by several factors which largely result from genetic predisposition, hereditary factors and the early appearance of microalbuminuria and/or systemic hypertension. Most of these factors are also implicated in the progression of nephropathy from microalbuminuria to overt proteinuria and to end-stage renal failure (ESRF). Over the last few years, the role of hyperglycaemia has emerged as critical in mediating the progressive renal damage in diabetes. However, hyperglycaemia leads to increased formation of glycated proteins which may act as promoters of progression by localizing in renal tissue. In addition, hyperglycaemia may have a synergistic effect with some other risk factors, such as growth factors and the renin angiotensin system, in accelerating renal deterioration.

A biochemical and bone biopsy investigation was made in 30 patients with chronic renal failure. Osteomalacia was the main pathological feature in 60% of the patients. Both optical and electron microscopic studies showed that the matrix adjacent to the osteoblasts was not mineralized. Osteomalacia was associated with increased osteoclastic activity and some degree of bone resorption and bone marrow fibrosis in 13% of the patients. In the remaining patients (27%) the bone tissue was substantially normal. The bone calcium content was lower than normal in uraemic patients, whereas a significant increase in magnesium content was observed.The low frequency of the pathological features specific for hyperparathyroidism may be explained by the low-protein, low-phosphorus diets usually followed by the patients. The decrease in bone calcium content depends probably on the reduction in its intestinal absorption and partly on the protein depletion usually observed in patients on low-protein diets. Furthermore, the bone magnesium excess may be regarded as a potentiating factor of bone calcium deficiency.

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