A number of abnormalities common in various types of kidney disease. Various forms of disorder that is often found in kidney disease is the presence of the cylinder which is a small piece of protein substance that settles on the tubules and passed into the bladder. Another important consequence of kidney disease is the loss of ability to concentrate or dilute urine, uremia, acidosis, and abnormal retention of Na +.
Proteinuria.
In many kidney disease and a benign condition, the permeability of the glomerular capillaries increased and protein found in the urine more than usual were very few (proteinuria). Most of the proteins are albumin and abnormalities often called albuminuria. Relationship with albuminuria glomerular membrane charge has been discussed above. Number ptotein in urine may be very high and especially in nephroses include, protein lost in the urine can exceed the speed of plasma protein synthesis by the liver. Hipoproteinemia caused reduces oncotic pressure and plasma volume is reduced, sometimes to dangerously low, while the edema fluid accumulate in the tissues.
A benign condition that causes proteinuria is a little understood changes in renal hemodynamics are normal in some individuals causing urinary protein formed when they are in good standing (orthostatic albuminuria). Urine is formed when the individual is lying does not contain protein.
Proteinuria.
In many kidney disease and a benign condition, the permeability of the glomerular capillaries increased and protein found in the urine more than usual were very few (proteinuria). Most of the proteins are albumin and abnormalities often called albuminuria. Relationship with albuminuria glomerular membrane charge has been discussed above. Number ptotein in urine may be very high and especially in nephroses include, protein lost in the urine can exceed the speed of plasma protein synthesis by the liver. Hipoproteinemia caused reduces oncotic pressure and plasma volume is reduced, sometimes to dangerously low, while the edema fluid accumulate in the tissues.
A benign condition that causes proteinuria is a little understood changes in renal hemodynamics are normal in some individuals causing urinary protein formed when they are in good standing (orthostatic albuminuria). Urine is formed when the individual is lying does not contain protein.
Loss of Concentration & Dilution
In kidney disease, the urine becomes less dense and frequent urine volume increases, causing the symptoms of polyuria and nocturia (waking sleep to urinate). The ability to form a dilute urine is often permanent, but the disease has advanced kidney into the urine osmolality remained, roughly the same as plasma osmolality, indicating that kidney function is lost pengencaran and concentration. The loss is due in part due to impaired counter current mechanism, but more importantly because adala loss nephron function. If one kidney is removed by surgery, the number of functioning nephrons is halved. Number osmol excretion was not reduced to this area, so the remaining nephrons must each memfiltrasi and excrete substances more active osmotic impacting called osmotic diuresis, the osmotic diuresis, urine osmolality close to plasma (see above), the same occurs when the number of functioning nephrons decreases because of an illness. Of course, if most of the nephrons are destroyed, reduced urine volume and occur oliguria or anuria.
Uremia
When the breakdown products of protein metabolism accumulate in the blood, there was a syndrome known as uremia. The symptoms of uremia are lethargy, anorexia, nausea and vomiting, mental disorders and mental disorders, and coma. Because suppressed erythropoiesis, anemia is a prominent picture of chronic uremia. Levels of blood urea nitrogen (BUN = Blood Urea Nitrogen), nonprotein nitrogen (NPN) and high creatinine levels, and the levels of these substances in the blood used weight segbagai Index uremia. Uremia often not preceded by the accumulation of urea and kreatnin own but accumulation of other toxic substances, probably organic acids or phenols that cause the symptoms of uremia. Because urea penetrate the blood-brain barrier slowly, urea given intravenously neurosurgical patients to make the outside of the brain CES hypertonic and shrink the brain during surgery. However, the infusion of urea causes changes in the electrical activity of the brain in animals and may not be as dangerous as it looks. In dogs, the old urea infusion causes anorexia, fatigue, muntah0muntah, and diarrhea.
Toxic substances are causing the symptoms of uremia can be removed by the blood of patients with kidney dialisisi artefisial with an appropriate arrangement. With repeated dialysis patients can be kept alive and healthy enough for a few months even though they are perfectly anuria or both kidneys had been removed.
Acidosis
Acidosis is often present in chronic kidney disease caused by the failure to excrete asm generated from the digestion and metabolism. In renal tubular acidosis syndrome, a rare, there is a specific disruption in the ability to make the urine acid and other renal function is usually normal. However, in most cases of chronic kidney disease, the most acidified urine and acidosis occurs because the total number of H + secretion can be reduced due to the failure of the tubuleskidneys to produce NH3.Abnormal metabolism of Na +
Many patients with kidney disease retain large amounts of Na + and to edema. At least there are three sebabretensi Na + in renal disease. In the glomerulus akuta, ie a primary effect on the disease glomerulus, there is a decrease in the amount of Na + filtered with virtually no decrease in Na + reabsorption. In nephroses include, increases aldosterone secretion helps water retention. Plasma proteins in these circumstances is low and fluid moves from the plasma into the interstitial space and plasma volume decreases. Decrease in plasma volume increases aldosterone secretion stimulated by the renin-angiotensin system.
The third cause of the Na + retention and edema in kidney disease is heart trouble. Kidney disease is a predisposing heart trouble partly because hypertension is often posed. Syndrome is a rare, but interesting is salt-losing nephritis. In this situation there is a loss of Na + in the urine very much, that can not be corrected by endogenous and exogenous mineralocorticoid and signs and symptoms of hypovolemia can make a wrong diagnosis edrenal cortical insufficiency. Ii syndrome is clearly due to selective damage relative to Na + reabsorption mechanism. In patients with these conditions, very high salt intake is necessary to prevent cardiovascular collapse.
Aldosterone Response Against Variation
An interesting problem is why aldosterone given in normal individuals and patients with hyper-aldosteronism undergo a severe shortage of K +, whereas patients edemadengan nephroses include, cirrhosis, or who suffer from heart trouble of secondary hyperaldosteronism.
One factor seems to be a number of Na + to the distal tubule. Na + in the tubular fluid to help maintain the potential difference between the tubular lumen and tubular cells and K + secretion is advantageous. In patients with primary hyperaldosteronism occurs "escape" and Na + reabsorption in the proximal tubule decreased, resulting in a large number of Na + to the distal tubule. In patients with edema, Na + filtered maybe a little because of low plasma Na + due to "dilution hyponatremia" or because of low GFR or both. However, the number of Na + reaching the distal tubule Na + may be low despite clear olasma and normal GFR because there is an increase Na + reabsorption in the parts of the more proximal nephron. Another factor in patients with edema is fluid flow in distal vessels. Excretion of K + seems to be limited by the flow and the sufferers is the amount of fluid to the distal tubule is often reduced.
