Renal parenchymal hypertension: relevant new aspects.

Renal parenchymal disease is the most common cause of secondary hypertension, accounting for up to 5% cases of all cases of systemic hypertension. Renal parenchymal hypertension occurs as a complication of a wide variety of glomerular and tubulointerstitial diseases and may aggravate the decline of kidney function. The pathophysiology of renal parenchymal hypertension represents a combined interaction of the impaired sodium handling leading to volume expansion, alteration of the renin-angiotensin system, abnormalities in endogenous vasodepressor compounds and possibly enhanced activity of vasoactive substances. Renal parenchymal hypertension can occur in acute and chronic kidney disease, manifesting early in the renal function impairment. It often requires complex pharmacological treatment of blood pressure and is prognostically unfavorable in terms of cardiovascular and renal complications. This form of secondary hypertension can often be successfully treated by therapy of the underlying renal disease. In case of insufficient blood pressure compensation, renal impairment progresses. The aim of this paper is to give a brief overview of renoparenchymatous hypertension, current diagnostic possibilities and principles of therapy.

Proteinuria from an internists point of view.

A basal level of proteinuria is about 30-100 mg/day, the upper limit of basal proteinuria does not exceed 150 mg/day which is considered non-pathology. Albumin accounts approximately 15 % of basal protein in the urine, other plasma proteins (immunoglobulins, β-2 microglobulin, Tamm-Horsfall mucoprotein) comprise the remaining 85 % of total quantity non-pathology proteinuria. Persistent proteinuria present for more than three months already meets the definition of chronic kidney disease independently of the stage of the estimated glomerular filtration rate. Patients are classified as A1-A3 based on the level of albuminuria. Examination of the albumin in the urine is one of the single sensitive indicators of chronic kidney disease. Proteinuria is an independent risk factor for cardiovascular disease, overall mortality and end stage renal failure both in general population and in population with chronic kidney disease. Presence of the urinary protein is associated with a higher mortality rate in critically ill patients. The degree of proteinuria after kidney transplantation predicts graft and patient survival in this population. Pharmacological and non-pharmacological treatments that attenuate proteinuria have been associated with better prognosis of kidney disease.

Proteinuria from an internists point of view.

A basal level of proteinuria is about 30-100 mg/day, the upper limit of basal proteinuria does not exceed 150 mg/day which is considered non-pathology. Albumin accounts approximately 15 % of basal protein in the urine, other plasma proteins (immunoglobulins, β-2 microglobulin, Tamm-Horsfall mucoprotein) comprise the remaining 85 % of total quantity non-pathology proteinuria. Persistent proteinuria present for more than three months already meets the definition of chronic kidney disease independently of the stage of the estimated glomerular filtration rate. Patients are classified as A1-A3 based on the level of albuminuria. Examination of the albumin in the urine is one of the single sensitive indicators of chronic kidney disease. Proteinuria is an independent risk factor for cardiovascular disease, overall mortality and end stage renal failure both in general population and in population with chronic kidney disease. Presence of the urinary protein is associated with a higher mortality rate in critically ill patients. The degree of proteinuria after kidney transplantation predicts graft and patient survival in this population. Pharmacological and non-pharmacological treatments that attenuate proteinuria have been associated with better prognosis of kidney disease.