Chronic renal failure

People with chronic renal failure and uremia show a constellation of symptoms, signs and laboratory abnormalities, in addition to those observed in acute renal injury. This reflects the nature of their long-standing renal failure and progressive and its effects on many types of tissues.

Therefore, osteodystrophy, neuropathy, bilateral kidneys showed little abdominal ultrasonography, and anemia are typical initial results suggest that a chronic course of a newlydiagnosis of the kidneys are not on the basis of elevated serum urea and creatinine.

One of the most typical causes permanent kidney failure is diabetes mellitus, hypertension and approved by glomerulonephritis. Polycystic kidney disease, obstruction and viruses are among the least typical causes of chronic renal failure. The pathogenesis of acute renal disease is very different from permanent kidney disease.

Whereas the acute injury of the kidney resultsand the change in the death of tubular epithelial cells, often followed by regeneration, with restoration of normal architecture, the damage results in irreversible loss of nephrons continues. As a result, a more practical burden is borne by a smaller number of nephrons, which manifests as an improvement in glomerular filtration pressure and hyperfiltration.

For factors not well understood, this compensation hyperfiltration, which may be thought of as a form of "high" levelEach nephron predisposes to fibrosis and scarring (glomerular sclerosis). As a result, the rate of destruction of nephron reduction and lift, thus accelerating the progression of uremia, the complex of symptoms and signs that occurs when the residual renal purpose is insufficient.

Thanks to the enormous reserve of the renal circulation, up to 50% of the nephrons can be lost with no evidence of short-term functional impairment. This is because people with two healthythe kidneys are able to donate for a single transplant. When GFR is reduced even more, leaving only 20% of the failure of the initial capacity, a degree of azotemia (elevation in blood vessels of the products normally excreted by the kidneys) is noticed.

However, asymptomatic patients may be in large part, simply because a new equilibrium is reached, in which blood vessels levels of such products are not high enough to cause overt toxicity. However, even in thisapparently stable level of late renal hyperfiltration evolution accelerated in chronic renal insufficiency in terminal stage is in progress.

Moreover, simply because individuals with this level of GFR is small reserve practice, which can easily become uremic with any additional power (eg, viruses, obstruction, dehydration, or nephrotoxic drugs) or any catabolic state associated with a higher turnover of nitrogen - containing products with reduced GFR.

L 'pathogenesis of renal failure following is based in part on the results of the poisonous mixture of 1) farm products (usually excreted by the kidneys (eg, nitrogen-containing objects in the metabolism of proteins), (2) the ordinary products such as hormones now present in large amounts, and (3) the lack of normal kidney products (eg, loss of erythropoietin).

excretory failure results in fluid shifts, increased intracellular Na + and water and decreasingIntracellular K +. These alterations may contribute to subtle alterations in the context of a series of enzymes, transport systems, and so on. Patients with chronic renal failure usually have some degree of Na + and water also, reflecting the loss of the route of renal excretion of water and salt.

A moderate degree of Na + and excess water, which could happen without objective indicators of excess extracellular fluid. However, excessive intake of Na + continues to contribute to failureheart failure, hypertension, ascites, peripheral edema and weight gain. On the other hand, excessive ingestion of drinking water contributes to hyponatremia.

A typical recommendation for the patient with renal failure remains is to avoid excessive salt intake and limiting fluid intake to ensure that it is equal to the production of urine and 500 ml (insensible losses). Other adjustments in the amount of the order may be made either through the use of diuretics (in a patient, however, urine) ordialysis.

Why are these people also have impaired renal mechanisms of salt and water conservation, the losses are much more sensitive than usual to sudden extrarenal Na + and water (eg, vomiting, diarrhea, sweating and fever). In these circumstances, much easier to create low ECF, the further deterioration of renal effects (which may not be reversible), and even circulatory collapse and shock.

Symptoms and indicators of dry mucous membranes,dizziness, syncope, tachycardia, jugular venous filling suggest that the progression of the decline in quantity. Hyperkalemia is a serious problem in chronic renal failure, especially for people whose glomerular filtration rate fell below 5 ml / min. Above that level, as GFR decreases, aldosterone-mediated K + transport in distal tubule-compensation increases.

Thus, a patient whose GFR is between 50 ml / min and 5 ml / min depending on tubular transport to maintain K + balance.Treatment with potassium-sparing diuretics, ACE inhibitors or blockers, drugs that can affect aldosterone-mediated K + transport may, therefore, precipitate dangerous hyperkalemia in an individual with chronic renal failure.

People with diabetes mellitus (the main trigger for continuous renal failure) may have a hyporeninemic hypoaldosteronism syndrome. This syndrome is really a situation where the lack of production of renin by the kidney reduces levels of angiotensin II andconsequently hinders the secretion of aldosterone.

As a result, people involved are able to offset the decline in GFR increased aldosterone-mediated K + transport and therefore have difficulty in movement of K +. This difficulty is usually manifested as hyperkalemia even before GFR has fallen below 5 ml / min.

Finally, not only patients with chronic renal failure much more sensitive to the effects of Na + overload or quantity, but also morerisk of hyperkalemia in the face of sudden loads of K + from both endogenous sources (eg, hemolysis, viruses, trauma) or exogenous sources (eg, blood vessels stored foods rich in K + or K + containing medicines).

The reduced ability to excrete acid and non-renal continuous basis to generate results in metabolic acidosis. In most cases when the GFR is above 20 ml / min, acidosis develops only reasonable time before returning to establish a new equilibrium of production and bufferuse. The decrease in pH of the blood vessels of these people usually can be corrected with 20-30 mmol (3.2 g) of sodium bicarbonate orally every day.

However, these people are extremely sensitive to acidosis in the case of a load of acid or sudden onset of problems that increase the acid load generated. Several problems of phosphate, Ca2 +, and bone metabolism can be seen in continuous renal not the result of a complex series of events.

Key factorsthe pathogenesis of these problems include: (1) a decrease in Ca2 + absorption in the intestine, (some) the overproduction of parathyroid hormone (three), disorders of metabolism of vitamin D, and (4) chronic metabolic acidosis . All these factors contribute to increased bone resorption.

Hypophosphatemia and hypermagnesemia can occur from excessive use of phosphate binders and antacids containing magnesium, but is more typical of hyperphosphatemia. Hyperphosphataemia contributes to improvinghypocalcemia, and then acts as a trigger for additional secondary hyperparathyroidism, raising the levels of PTH in the blood.

The elevated PTH blood vessels further reduces bone Ca 2 +, and contributes to chronic renal osteomalacia (see below). Congestive heart failure and pulmonary edema can develop in a context of overload and salt.

Hypertension is a typical finding in chronic renal failure, also, in general, based on fluid and Na +overload. However, hyperreninemia also recognized as a syndrome that includes renal perfusion triggers kidney failure excess renin and thus increase systemic blood pressure.

Pericarditis caused by irritation and inflammation of the pericardium by uremic toxins is a complication whose incidence in continuous renal failure is decreasing due to the institution before kidney dialysis. Increased cardiovascular risk is a complication in patients with chronic diseasesrenal failure and is causing mortality in this population.

Is the result of a heart attack, stroke and peripheral vascular disease. Cardiovascular risk factors in these patients are hypertension, hyperlipidemia, glucose intolerance, chronic increase in cardiac output, and myocardial and valvular calcification is a consequence of increased Ca2 + PO43 product x, and other, less well-characterized uremic environmental factors.

People withcontinuous renal failure have marked abnormalities in red blood cells, white blood vessels purpose and parameters of coagulation. Normochromic, normocytic anemia, with signs and symptoms of apathy and fatigue easily and hematocrit levels typically in the range of 20-25%, is a constant feature.

The anemia is due to the lack of production of erythropoietin and the lack of its stimulating effect on erythropoiesis. Therefore, people with chronic renal failurefailure, regardless of the position of dialysis, show a marked improvement in hematocrit during treatment with erythropoietin (epoetin alfa).

Other causes of anemia can include bone marrow suppression effects of uremic toxins, bone marrow fibrosis of blood vessels due to elevated PTH, the toxic effects of aluminum (in antacids, phosphate binder and dialysis solutions) and hemolysis and blood loss associated with dialysis (while the individual is an anticoagulantheparin).

People with chronic renal failure show abnormal hemostasis manifested as high-shock, blood vessels increased reduction surgery, and a high incidence of spontaneous gastrointestinal hemorrhage and cerebrovascular disease (including cerebral hemorrhage and subdural hematoma).

Laboratory abnormalities include prolonged bleeding time, decreased platelet factor III, platelet aggregation and adhesion abnormal prothrombin and the use of altered, none of this iscompletely reversible, even in well-dialyzed individuals. Uremia is associated with high susceptibility to infection, which is considered due to the removal of leukocytes from uremic toxins.

The deletion seems to be greater for neutrophils and lymphoid cells also appear to affect the chemotaxis, the acute inflammatory response, delayed hypersensitivity and the functions of most leukocytes. Acidosis, hyperglycemia, hyperosmolarity and malnutrition are also consideredcontribute to the immunosuppressive therapy, permanent renal failure.

The invasion of dialysis and the use of immunosuppressive drugs in kidney transplant patients also contribute to an increased incidence of infections. CNS signs and symptoms and indicators could range from sleep disorders and mild mental impairment of concentration, poor memory, misjudgments, and neuromuscular irritability (manifested as hiccups, cramps, twitches and spasms) for asterixis, myoclonus,stupor, convulsions and coma in terminal uremia.

Asterixis manifests as involuntary movements seen when the arms are flapping open and grabbed her wrists to "stop the visitors." due to altered E 'of nerve conduction in metabolic encephalopathy wide range of causes, including kidney failure.

Peripheral neuropathy (sensory motor, lower extremities than the upper), exemplified by the Restless Legs Syndrome (feeling sick and poorly localizedinvoluntary movements of limbs), is a common finding continued deterioration in the absence of an important indication for starting dialysis.

Patients undergoing hemodialysis may develop aluminum toxicity, characterized by speech dyspraxia (inability to repeat words), myoclonus, dementia and seizures. Similarly, aggressive acute dialysis can result in a disequilibrium syndrome is characterized by nausea, vomiting, drowsiness, headache, seizures, and within an individual with realityHigh BUN value.

Presumably, this really is an impact of pH or osmolality rapid change in the ECF, resulting in cerebral edema. Nonspecific GI results in uremic patients include anorexia, hiccups, nausea, vomiting, and diverticulosis. Although its exact pathogenesis is unclear, many of the best results with dialysis. Woman with uremia have reduced the amount of estrogen, which may explain the high incidence of amenorrhea and the observation that almost never are able to to end a pregnancy.

regular periods, but higher production rate of pregnancy in general, he took frequent dialysis. Similarly, low levels of testosterone, impotence, oligospermia, and germinal cell dysplasia were common in men with renal continuous no. Finally, continuous renal failure kidney removed as a site of degradation of insulin, which increases the half-life of insulin.

This usually has a stabilizing effect in diabetic patients> Blood sugar was previously difficult to control. Skin changes result from many of the results of continuous renal currently under discussion.

Renal failure patients may still show pallor due to anemia, abnormal skin color related to metabolites accumulated pigmented or gray resulting from hemochromatosis, transfusion-mediated, bruising and hematomas as a result of bleeding disorders, and itching and excoriation resultCa2 + stores secondary hyperparathyroidism. Finally, when urea concentrations are much higher, the evaporation of sweat leaves a residue of urea called "uremic frost."