Renal parenchymal hypertension

Intravascular volume expansion is a major pathogenic factor in renal parenchymal hypertension. In these patients, excessive renin secretion relative to volume status and heightened sympathetic nerve activity are observed, and those contribute to hypertension in patients with renal injury. Potential mechanisms include afferent stimuli from the injured kidneys to the brain, reduced central dopaminergic tone, reduced baroreceptor sensitivity, abnormal vagal function and endothelial dysfunction in patients with renal dysfunction [45, 46, 49],... 

Most progressive nephropathies share a final common pathway to irreversible renal parenchymal damage and ESRD (Fig. 76-1). Key pathway elements are loss of nephron mass, glomerular capillary hypertension, and proteinuria. 

The clinical manifestations of gout, i.e. articular and renal disease, are intimately connected with hyperuricemia and/or particularities of renal handling of uric acid. It is well established that normalization of plasma uric levels will cure the joint disease. The diminution of renal uric acid excretion by administration of allopurinol will cure nephrolithiasis in its uncomplicated forms. One may presume that the other manifestations of the gouty kidney (i.e. parenchymal renal disease, hypertension and azotemia) will also be influenced by a therapy reducing urinary uric acid however no reliable reports exist as yet on this point. 

Thus, in general, most hypertensive patients have essential hypertension or other better known forms of secondary hypertension that could include renovascular h5 ertension (due to renal artery stenosis), or chronic renal insufficiency (due to renal parenchymal disease), adrenal or steroid abnormalities (due to... 

Soon after the introduction of ACEl much attention was given to their renal side effects. This initiated a lot of research, especially because hypertension frequently is present in patients with renal vascular and/or parenchymal disease and the use of ACEl therefore was... 

Patients with chronic parenchymal renal disease show a fall in RBF and GFR during treatment with NSAID, including aspirin . In chronic glomerulonephritis, afferent arteriolar dilatation may be a compensatory mechanism in the maintenance of filtration. A study of patients with systemic lupus erythematosus revealed an abnormal increase in basal PGE2 excretion consistent with the postulated means of compensation. In other aetiologies of renal insufficiency, including diabetes, hypertension and interstitial nephritis, there is acute worsening of renal function with NSAID " ... 

Specific chapters deal with agenesis, dysplasia, parenchymal diseases, neoplastic diseases, stone disease, vascular hypertension, renal failure and renal transplantation and genitourinary trauma in children. Specific problems of childhood neurogenic bladder are discussed. 

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