Warung Bebas

Thursday, 13 October 2011


Pathophysiology of CKD at first depending on the underlying disease, but in the later development process that occurs more or less the same, a chronic progressive in the long run will cause a decrease in renal mass. In line with the decrease of renal mass, as a compensation mechanism that is still better then the nephron hyperfiltration therefore will experience an increase in glomerular capillary pressure and flow, and subsequent hypertrophy. Structural and functional hypertrophy of residual nephrons is still good is happening due to the influence of vasoactive molecules, cytokines and growth factor, and eventually will happen sclerosis process. Renin-action activities intravenous Angiostensin also played a role in the occurrence of hiperfilltrasi-hypertrophy and sclerosis.

 Pathophysiology that occur include:
a. Azotemia toxic (toxic metabolites)
          If there is a decrease in glomerular filtrate rate just happened retention of some toxin azotemia (U, metilguanidin, GSA). For example, GSA (guanidinosuccinic acid), these substances inhibit ADP (adenosine diphosphate) used to release platelet factor 3, so it will cause coagulation disorders.
           Although urea and serum creatinine concentration is used to measure the renal excretory capacity, the accumulation of both the molecule itself does not explain many of the symptoms and signs that characterize uremic syndrome in advanced renal failure. Hundreds of toxins that accumulate in renal failure has been involved in the uremic syndrome. These include water-soluble, hydrophobic, protein bound, charged, and uncharged compounds. Additional categories include nitrogen excretory products guanido compounds, veining and hippurates, products of the metabolism of nucleic acids, polyamines, myoinositol, phenol, benzoate, and indoles. Compounds with molecular mass between 500 and 1500 Da, which is called middle molecules, was also detained and contribute to morbidity and mortality.
           Uremic syndrome and disease state associated with renal impairment, automatically involves more than excretory renal failure. A number of metabolic and endocrine functions normally performed by the kidneys are also affected, and this results in anemia, malnutrition, and abnormal metabolism of carbohydrates, fats, and proteins. In addition, plasma levels of hormones, including PTH, insulin, glucagon, sex hormone, and prolactin, changes in renal failure as a result of urinary retention, decreased degradation, or abnormal regulation. Finally, progressive renal impairment was associated with worsening of systemic inflammation. Elevated levels of C-reactive protein was detected along with acute phase reactants, while the level of so-called negative acute phase reactants, such as albumin and fetuin, decreased with progressive renal damage. Thus, renal impairment is important in malnutrition-inflammation-atherosclerosis/calcification syndrome, which in turn contributes to the acceleration of vascular disease and comorbidities associated with advanced kidney disease.
         In summary, the pathophysiology of uremic syndrome can be divided into manifestation in the three areas of dysfunction: (1) consequent to the accumulation of toxins normally experienced renal excretion, including their protein products of metabolism, (2) consequent to the loss of others renal function, such as fluid homeostasis and electrolyte and hormonal regulation, and (3) progressive systemic inflammation and vascular and nutritional consequences

b. Trade-off hypothesis (intact nephron hyphothesis)
         According to this concept, the whole kidney physiology will be taken by the nephrons are still intact. In these nephrons have increased the concentration of solutes such as urea, resulting in osmotic diuresis to remove urea per minute which resulted in increased urine volume. This compensatory mechanism aimed at maintaining body fluid balance (homeostasis).
c. Metabolic disorders
1) Metabolism of carbohydrate
Mechanism of glucose intolerance is not known, suspected of having ties with the toxin azotemia. This hypothesis is based on the fact that glucose intolerance clinic can be corrected with intermittent hemodialysis.
2) Metabolism of fat
Hypertriglyceridemia occurs in patients with chronic renal failure undergoing intermittent hemodialysis. The mechanism is unknown, allegedly due to increased synthesis of triglyceride-rich lipoproteins in the liver.
3) Metabolism of proteins
In the normal restrictions on the amount of protein in a long time can cause a negative balance of nitrogen. In contrast to patients with CKD restrictions on the amount of protein in the menu will not cause a negative balance of nitrogen.
4) Metabolism of uric acid
Hyperuricaemia is common in CKD, although the increase in serum uric acid has no relation with the degree of decline in renal physiology. For the process is still not clear.
5) Electrolyte Metabolism
a)      Metabolism of Na
Natriuretic hormone or suspected presence of factors that inhibit reabsorption of sodium ions in the renal tubules causing increased excretion of sodium. When the renal physiology continued to deteriorate with decrease in nephron-nephron number that is still intact, increased natriuresis.
b)      Water Metabolism
In some patients with CKD by increasing the number of nephrons is reduced, flexibility for the excretion of water will also be reduced so easily happen poisoning of water (water overload) both renal and extra renal causes hyponatremia.
c)      Metabolism of potassium
Hypokalemia can be found in patients with CKD caused by poor dietary potassium, a powerful diuretic that is not controlled, secondary hyperaldosteronism from volume depletion and tubular diseases such as Fanconi syndrome, and because of interstitial nephritis.
d)     acid-base balance
Pathogenesis of metabolic acidosis in CKD are:
(1) decrease the excretion of ammonia due to loss of nephron number.
(2) decrease the excretion of titrable acid, especially phosphate, because the intake and absorption through the intestines is reduced.
(3) Loss of a number of bicarbonate through the urine (bicarbonate wasting).
e) Calcium Metabolism
In patients with CKD often found hypocalcemia, due to decreased Ca absorption through the gut and impaired mobilization of Ca and hyperphosphatemia.
e)      Phosphorus
f)   Hyperphosphatemia that occurs in CKD plays an important role to arise hypocalcemia and hyperparathyroidism, and ultimately can cause the spread of calcification in other organs (metastatic calcification).
g)       Magnesium
The increase in serum magnesium very rarely cause complaints or symptoms, except for magnesium-containing antacids laxative and will suppress the Central Nervous System.

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