A qualitative and quantitative analysis of urinary lipids in the nephrotic syndrome is presented. The following lipids were identified in the urine of patients with the nephrotic syndrome: free cholesterol, cholesterol esters, triglycerides, free fatty acids, and phospholipids. Glass paper chromatography identified the cholesterol esters as palmitate, oleate, linoleate, and arachidonate, and identified the phospholipids as phosphatidylcholine, phosphatidylethanolamine, and phosphatidylserine. Urinary lipid excretion was much greater in patients with the nephrotic syndrome than in patients with chronic renal disease and minimal proteinuria, or in patients with hyperlipidemia from other causes. Urinary lipid excretion varied widely among the 13 patients with the nephrotic syndrome studied, and no quantitative correlation with serum lipid levels was observed. However, qualitatively at least, the proportion of cholesterol esters excreted in the urine was similar to the proportion of these esters in plasma. A good correlation was found between lipid excretion and glomerular permeability. Furthermore, during steroid therapy urinary lipid excretion decreased concomitant with a decrease in proteinuria. All these observations support the idea that lipiduria in the nephrotic syndrome is related to protein loss and that most of the lipid in the urine enters the glomerular filtrate in the form of lipoproteins.

Adolescent↗

PubMed1966

Effects of dinitrophenol and oligomycin on the coupling between anaerobic metabolism and anaerobic sodium transport by the isolated turtle bladder.

Dinitrophenol (1 x 10(-5)M) has been found to inhibit anaerobic sodium transport by the isolated urinary bladder of the fresh water turtle. Concurrently, anaerobic glycolysis was stimulated markedly. However, tissue ATP levels diminished only modestly, remaining at approximately 75% of values observed under anaerobic conditions without DNP. The utilization of glucose (from endogenous glycogen) corresponded closely to that predicted from the molar quantities of lactate formed. Thus the glycolytic pathway was completed in the presence of DNP and if ATP were synthesized normally during glycolysis, synthesis should have been increased. On the other hand, the decrease in Na transport should have decreased ATP utilization. Oligomycin did not block sodium transport either aerobically or anaerobically, but ATP concentrations did decrease. When anaerobic glycolysis was blocked by iodoacetate, pyruvate did not sustain sodium transport thus suggesting that no electron acceptors were available in the system. Two explanations are entertained for the anaerobic effect of DNP: (a) Stimulation by DNP of plasma membrane as well as mitochondrial ATPase activity; (b) inhibition of a high energy intermediate derived from glycolytic ATP or from glycolysis per se. The arguments relevant to each possibility are presented in the text. Although definitive resolution is not possible, we believe that the data favor the hypothesis that there was a high energy intermediate in the anaerobic system and that this intermediate, rather than ATP, served as the immediate source of energy for the sodium pump.

Adenosine Triphosphatases↗

PubMed1966

The functional adaptation of the diseased kidney. 3. Ammonium excretion.

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Ammonia↗

PubMed1966

Evaluation of renal function in malnutrition.

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Acute Kidney Injury↗

PubMedDate not supplied

Progression of chronic renal disease.

Progressive chronic renal disease is characterized histologically by the accumulation of extracellular matrix proteins within the renal interstitium and progressive tubular atrophy. A number of kidney diseases and their progression to end-stage renal failure are driven by the intercrine, autocrine, paracrine, and endocrine effects of angiotensin II. Growth factors appear to have an important role in the development and progression of diabetic nephropathy. Substantial evidence indicates that induction of transforming growth factor beta (TGF-beta) is mediated by high levels of glucose. TGF-beta is pivotal for the hypertrophy of mesangial and tubular cells. Other factors such as hypertension, protein glycation products, and other mediators may further amplify the synthesis of TGF-beta and/or the expression of its receptors in the diabetic state. Other cytokines, such as tumor necrosis factor alpha also contribute to the progression of chronic renal disease. The overall picture derived from several studies of chronic renal disease suggests that treatment of the progression of the renal fibrosis may require the use of several strategies to prevent the advent of end-stage renal disease.

Angiotensin II↗

PubMedDate not supplied

Mechanisms of progression of chronic renal damage.

The amount of protein in the urine is a strong predictor of subsequent loss of renal function. Proteinuria and tubular atrophy have been linked with progressive renal insufficiency. In the last few years several studies have indicated that smoking is also a risk factor in the progression of renal disease. In addition, a number of studies have suggested that higher levels of blood pressure are associated with a faster decline in renal function. A number of cytokines, vasoactive compounds, chemoattractant molecules and growth factors are upregulated during the course of progressive renal disease in experimental animals. Recent data indicate that vasoconstrictor substances have a key role in the initial phases of this process. In particular, angiotensin II is increased following the development of renal injury. Angiotensin in turn upregulates the expression of other factors including: transforming growth factor beta, tumor necrosis alpha, nuclear factor kappaB and several chemoattractant compounds. Other vasoactive compounds (endothelin, thromboxane A2 and prostaglandins) may also be upregulated during the course of progressive renal disease

Angiotensin II↗

PubMedDate not supplied

Progression of chronic renal disease.

Chronic diseases of the kidney are characterized by progression once a certain portion of renal function is lost. End-stage kidneys, the result of progressive chronic renal disease, are characterized by sclerosis, tubulointerstitial scarring, and collapse of glomerular capillary tufts. The mechanisms and risk factors responsible for the progression of renal disease have been studied intensively in the past decade, and it now appears that multiple nonimmunologic factors are responsible. These factors include systemic hypertension, hyperlipidemia, proteinuria, excessive intake of protein, and adaptive changes in nephron function as a consequence of nephron loss. The latter adaptations, increased intraglomerular pressure, increased excretion of ammonia, "hypermetabolism," decreased afferent arteriolar tone, and renal hypertrophy, may also be responsible for the progression of renal disease. A complete understanding of the factors responsible for the progression of renal disease should permit rational development of appropriate therapeutic interventions.

Humans↗

PubMedDate not supplied

The role of calcium in renal gluconeogenesis: studies using ionophore A23187.

The divalent cation ionophore A23187 was found to increase glucose production from alpha-ketoglutarate, glutamine, succinate, and lactate but not from glycerol in isolated rat renal cortical tubules at external Ca++ concentrations of 0.1 mM. At an external Ca++ concentration of 1.0 mM or in the absence of external Ca++, the ionophore did not increase glucose production from alpha-ketoglutarate. Ionophore A 23187 did not increase cyclic AMP levels in renal cortical tubules or slices. The increase in glucose production produced by ionophore A23187 was completely prevented by pre-incubation of the tubules with 10(-5) M pentobarbital, a known inhibitor of calcium transport in biological systems. The experiments suggest that ionophore A23187 increases gluconeogenesis from a variety of substrates by altering the levels of cytosolic calcium without affecting the concentrations of cyclic AMP.

Animals↗