Uremia Chronic renal disease

Patients with either acute or chronic renal failure may present with many and varied manifestations of uremia [12]. In these patients, the application of biomarkers of effect to detect clinical disease in its earliest stages is of great importance. Table 2 contains a list of various groups of xenobiotics associated with acute or chronic renal disease. 

Chronic renal failure Is treated by dialysis, kidney transplants, and drugs, as well as by Sow-protein diets. For tlris reason, an outline of chronic renal failure occurs in this chapter. The normal giomernlar filtration rate (GFR) is 80 to 120 ml/min. In severe renal disease, the GFR can be reduced to 10 ml/min or less. This represents a 90% loss of renal function. Diabetes mellitus and hypertension thigh blood pressure) are the main causes of chronic renal failure. Sustained and chronic injury to the kidneys leads to the destruction of the nephrons, where this destruction is usually not reversible. The nephron, which is the sm a I lest unit of kidney function, isdtjtailEd in the section on dium, Potassium, Chloride, and Water. The severe loss of nephrons results in alterations of functions of many other organs of the body. The collechon of abnormalities that results is called uremia. 

Long-term use of calcium salts can cause the milk-alkali syndrome and alkalosis in conjunction with hypercalcemia and renal insufficiency (6). It presents acutely with headache, nausea, irritability, and weakness, or chronically with uremia, alkalosis, and hypercalcemia. Sustained high dosage and/or concurrent renal disease are common antecedents (7). 

As Balkan nephropathy is characterized with slow asymptomatic course, most authors identify two main stages of the disease the first, asymptomatic (latent, subclinical) and second, manifest (symptomatic). The latter is usually subdivided into the stage without renal failure (early, compensated Balkan nephropathy, with no azotemia) and chronic renal failure (decompensated Balkan nephropathy, uremia) [19,88, 89]. 

Marked elevations of plasma peptide hydroxyproline have been observed by Dubovsky et al. in chronic renal failure (D7). The highest levels were seen when uremia and severe bone disease occurred together. Removal of the parathyroids in four patients (three primary and one secondary hyperparathyroidism) was associated with return to normal levels when renal function was normal, and significant reduction when renal failure was present. It seems possible that plasma peptide hydroxyproline might be a rapidly changing and sensitive indicator of bone metabolism which could be studied even with renal impairment, a major obstacle to most current techniques in the diagnosis of hyperparathyroid states. 

Clinicians rely mainly on blood urea nitrogen (BUN) and serum creatinine measurements to evaluate patients with renal failure. Yet the correlation between symptoms and blood levels is at best approximate. In acute renal failure the underlying disease and its associated complications often dominate the clinical picture and determine the prognosis, and it is unclear at what level of nitrogen retention symptoms may be attributed to uremia. Clinicians generally institute dialysis when the BUN exceeds 100 mg/dl or the serum creatinine exceeds 10 mg/dl, but sometimes earlier or later, and early dialysis has not been shown to confer distinct benefits. In chronic renal failure, patients may be quite asymptomatic despite very high BUN and serum creatinine levels. Many so called uremic symptoms may be more properly attributed to anemia, heart failure, nephrotic edema and hypoproteinemia, hypertension, malnutrition, or uncontrolled diabetes or its complications, such as gastroparesis, diarrhea, and neuropathy. 

Levels of plasmalogens are decreased in several neurological disorders including Alzheimer s disease, ischemia, and spinal cord trauma. This decrease may be due to the stimulation of plasmalogen-selective PLA. A deficiency of plasmalogens in peroxisomal disorders and Niemaim-Pick type C disease indicates that this deficiency may be responsible for neurological dysfunction in these disorders. Plasmalogens are also involved in bronchopulmonary dysplasia, uremia, and chronic renal failure. 

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