The capacity of microalbuminuria to predict an increased cardiovascular and renal risk is well established in diabetic patients, as well as in essential hypertensive patients and in general population. Detection of microalbuminuria could then be relevant to select specific therapeutic strategies for reducing or preventing cardiovascular events in patients with essential hypertension. Microalbuminuria is detectable in almost 40% of the population with established hypertension, particularly in those patients not controlled satisfactorily with medical therapy. Albuminuria may represent a marker of renal damage and cardiovascular risk in essential hypertension. Microalbuminuria seems to represent a simple and reproducible method to better define cardiovascular risk profile in the hypertensive patient and to stratify the prognosis in relation to renal and cardiovascular risk. ACE-inhibitors and more recently angiotensin II receptor antagonists seem to exhibit a more market capacity to reduce microalbuminuria in patients with essential hypertension or diabetes mellitus. Determination of this parameter in daily clinical practice could facilitate the stratification of risk as well as the choice of therapy in essential hypertensive patients.

Albuminuria↗

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Effect of furosemide on renal function in the stenotic and contralateral kidneys of patients with renovascular hypertension.

In a group of six patients diagnosed as having unilateral renovascular hypertension due to fibromuscular dysplasia, inulin glomerular filtration rate, (GFR) and PAH renal plasma flow, (RPF) clearances, urine flow (V), urine sodium (UVNa), potassium (UVK), urinary excretion of prostaglandin E2 (UVPGE2), thromboxane B2 (UVTxB2), and 6-keto prostaglandin F1 alpha (UVPGF1 alpha) were measured in each kidney before and after the i.v. administration of furosemide (20 mg). The basal values of GFR, RPF, UVNa, UVPGE2, UVTxB2, and UV6-keto-PGF1 alpha were lower (p less than 0.01) in the stenotic kidney. Furosemide increased RPF 11% and 50%, GFR 25% and 62%, and V 142% and 280% in the contralateral and stenotic kidney respectively. The increase of UVNa was similar in the two kidneys. In the stenotic kidney, both UVPGE2 and UV6-keto-PGF1 alpha increased significantly (p less than 0.01) with furosemide while UVTxB2 remained unchanged. Furosemide did not alter the rate of excretion of the three prostaglandins measured in the contralateral kidney. We conclude that furosemide significantly improves renal circulatory and excretory function of the stenotic kidney. Since prostaglandin excretions also increased, the vasodilatation in the stenotic kidney may be prostaglandin mediated.

Adult↗

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Can the kidney prevent cardiovascular diseases?

The kidneys play an important role in the development of cardiovascular risk factors. It is well known that heavy proteinuria can induce hyperlipidemia, the uric acid is elevated in some renal deficiencies and that hypertension develops in most end stage renal diseases. In prehypertensive states, specially in subjects with a family history of hypertension, some hemodynamic changes take place, characterized by an increase in renal vasoconstriction with a reduction in renal plasma flow and an elevation of sodium reabsorption. The mechanisms for these alterations are not well understood, but an increase in intracytosolic calcium in vascular smooth muscle cells, a reduction in vasodilatory substances such as nitric oxide and an increased sympathetic nervous activity have been proposed. In normotensive subjects with two hypertensive parents a reduction in sodium diet, an increase in protein intake or in arginine diet could prevent established essential hypertension from developing. In borderline hypertension an early therapy with low doses of calcium antagonists, ACE inhibition or diuretics could be indicated.

Animals↗

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Renal surrogates in essential hypertension.

The kidney can be considered both as culprit and victim in the hypertensive process. Renal functional derangement contributes to the development of arterial hypertension and the development of secondary vascular damage both at the glomerular and arteriolar level accounts for the development of progressive nephrosclerosis. The most common alteration of renal function observed in humans since the early stages of essential hypertension is the presence of renal vasoconstriction. This can be accompanied by the appearance of hyperuricemia, increased urinary excretion of enzymes such as N-acetyl-beta- glucosaminidase and of proteins like albumin and beta2-microglobulin. Later on, a progressive fall in glomerular filtration rate accompanied or not by proteinuria can be observed if high blood pressure persists.

Albuminuria↗

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[Diagnostic and clinical course features of lupus membranous glomerulonephritis].

BACKGROUND: Lupus membranous glomerulonephritis (LMG) is sometimes difficult to distinguish from idiopathic membranous glomerulonephritis (IMG) and little is known about its natural history. METHODS: We have performed a retrospective study of 16 patients with LMG, types Va ("pure" LMG) (8 patients) and Vb (mesangial proliferation) (8 patients). Analytical and clinical characteristics were analyzed in each case at the onset of the disease and during follow-up. RESULTS: At the time of diagnosis, 7 patients (43%) did not present any extrarenal manifestations of systemic lupus erythematosus (SLE). Nephrotic syndrome was the most common clinical presentation (81%). 14 patients (87%) showed positive antinuclear antibodies (ANA), but at low titres (< 1/300); anti-DNA antibodies were positive only in 3 cases (18%) and hypocomplementemia was observed in 2 (12%). The most relevant histological findings were the presence of Clq deposits (83%) and subendothelial and mesangial deposits. Treatment consisted of corticosteroids, adding immunosuppression when no response was obtained in 2-3 months. In recent years, an angiotensin-converting enzyme inhibitor (ACEI) was added before immunosuppression. At the end of the study, 6 patients (42%) developed chronic renal insufficiency and 8 (58%) renainea with normal renal function. Actuarial renal survival was 100% at 5 years and 75% at 10 years. The evolution towards a non-nephrotic range proteinuria throughout the follow-up was the only parameter significantly associated with a good prognosis. CONCLUSIONS: LMG can present without extra-renal symptoms of SLE and even with very poor expression of its serological markers. Almost half of the patients (42%) developed chronic renal insufficiency. The evolution towards a non-nephrotic range proteinuria correlated with the maintenance of a normal renal function.

Adult↗

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[The value of high dose steroid therapy in obstructive uropathy caused by a tumor].

The case of an 82-years old female patient with acute renal failure secondary to tumoral obstructive uropathy by neoplasic invasion of the trigone is described. The condition was treated with urinary deviation through percutaneous nephrostomy of the left kidney which achieved an improvement in the renal function. Later, the percutaneous nephrostomy was unintentionally moved not being possible to place a new one in none of the kidneys. The patient remained anuric for 24 hours, and therapy was then instaured with high doses of intravenous steroids (6 Metyl-Prednisolone 1.5 g I.V. in 24 hours), diuresis was recovered and renal function became normalized within a few days. The mechanism of action and therapeutic usefulness of high dosage steroids in tumoral obstructive pathology is discussed.

Aged↗

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