Causes Symptoms Of Kidney Disease
Published on Apr 21 2010, in the categories: Symptoms Of Kidney Disease
This is an article on causes and symptoms of kidney disease. From all the possible options of causes and symptoms of kidney disease I decided to talk about renal failure. The chronic renal failure (CRF) may be caused by any major cause of renal dysfunction (see Table 222-3). The most common cause of end stage renal disease was diabetic nephropathy, followed by hypertensive nefroangiosclerosis and various primary and secondary glomerulopathy.
The functional effects of CRF can be summarized in: decreased renal reserve, renal failure and uremia. The concept of functional adaptation impairment explains why a loss of 75% of renal tissue produces only a fall of 50% compared to the standard of GFR. With less impairment reserves there is a measurable loss of renal function, but homeostasis is maintained at the expense of some hormonal adaptations (e.g. secondary hyperparathyroidism and changes intrarenal balance glomerulotubulare).
Plasma concentrations of creatinine and urea (which are highly dependent on glomerular filtration) begin to increase non-linearly when the GFR decreases. Alterations in the concentrations of creatinine and urea do not occur in the early stages, when the GFR falls below 6 ml/min/m2; levels rise rapidly and are usually associated with systemic manifestations (uremia). For substances that are excreted primarily by the secretion from the distal nephrons, adaptation usually results in normal concentrations insufficient to advance.
Despite the decline in GFR, the water balance and Na is well preserved by the increasing fraction of Na excretion and a normal response to thirst. Thus, the plasma concentration of Na is typically normal and hypervolemia is infrequent despite unchanged Na intake in the diet. However, imbalances can occur if the intake of Na and liquid is very limited or excessive.
Neuromuscular aspects include coarse muscle twitching, peripheral neuropathy with sensory and motor phenomena, muscle cramps and seizures (usually the result of hypertensive encephalopathy or metabolic). Anorexia, nausea, vomiting, stomatitis and halitosis are almost uniformly present. The dominant aspect of uremia and chronic malnutrition is leading to tissue destruction.
Advanced of IRC are frequent ulcers and GI bleeding. 80% of patients with advanced renal failure, you have hypertension which is usually related to ipervolemia and sometimes activation of the renin-angiotensin-aldosterone system. Heart disease (hypertension, ischemic) and renal Na and water retention can cause congestive heart failure or edema. Pericarditis, which is frequently observed in uremia chronic uremia can present acute, potentially reversible.
The skin may appear yellow-brown; sometimes urea from sweat may crystallize on the skin as a uremic frost. For some patients, the itching is particularly troublesome. The renal osteodystrophy (abnormal bone mineralization due to hyperparathyroidism, calcitriol deficiency, high serum phosphorus or Ca low or normal serum) usually takes the form of bone disease hyperparathyroidism (osteitis fibrosis).
Osteomalacia from chronic exposure to aluminum salts as phosphate binders and dialysate contamination was once common but now has fallen to about 5% of cases. The dominant form and an increase of renal osteodystrophy is adynamic bone disease, the predominant bone lesion in peritoneal dialysis (60%) hemodialysis patients, a prevalence comparable to that of the host fiber (about 36% versus 38 %).
The functional effects of CRF can be summarized in: decreased renal reserve, renal failure and uremia. The concept of functional adaptation impairment explains why a loss of 75% of renal tissue produces only a fall of 50% compared to the standard of GFR. With less impairment reserves there is a measurable loss of renal function, but homeostasis is maintained at the expense of some hormonal adaptations (e.g. secondary hyperparathyroidism and changes intrarenal balance glomerulotubulare).
Plasma concentrations of creatinine and urea (which are highly dependent on glomerular filtration) begin to increase non-linearly when the GFR decreases. Alterations in the concentrations of creatinine and urea do not occur in the early stages, when the GFR falls below 6 ml/min/m2; levels rise rapidly and are usually associated with systemic manifestations (uremia). For substances that are excreted primarily by the secretion from the distal nephrons, adaptation usually results in normal concentrations insufficient to advance.
Despite the decline in GFR, the water balance and Na is well preserved by the increasing fraction of Na excretion and a normal response to thirst. Thus, the plasma concentration of Na is typically normal and hypervolemia is infrequent despite unchanged Na intake in the diet. However, imbalances can occur if the intake of Na and liquid is very limited or excessive.
Neuromuscular aspects include coarse muscle twitching, peripheral neuropathy with sensory and motor phenomena, muscle cramps and seizures (usually the result of hypertensive encephalopathy or metabolic). Anorexia, nausea, vomiting, stomatitis and halitosis are almost uniformly present. The dominant aspect of uremia and chronic malnutrition is leading to tissue destruction.
Advanced of IRC are frequent ulcers and GI bleeding. 80% of patients with advanced renal failure, you have hypertension which is usually related to ipervolemia and sometimes activation of the renin-angiotensin-aldosterone system. Heart disease (hypertension, ischemic) and renal Na and water retention can cause congestive heart failure or edema. Pericarditis, which is frequently observed in uremia chronic uremia can present acute, potentially reversible.
The skin may appear yellow-brown; sometimes urea from sweat may crystallize on the skin as a uremic frost. For some patients, the itching is particularly troublesome. The renal osteodystrophy (abnormal bone mineralization due to hyperparathyroidism, calcitriol deficiency, high serum phosphorus or Ca low or normal serum) usually takes the form of bone disease hyperparathyroidism (osteitis fibrosis).
Osteomalacia from chronic exposure to aluminum salts as phosphate binders and dialysate contamination was once common but now has fallen to about 5% of cases. The dominant form and an increase of renal osteodystrophy is adynamic bone disease, the predominant bone lesion in peritoneal dialysis (60%) hemodialysis patients, a prevalence comparable to that of the host fiber (about 36% versus 38 %).
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