Chronic kidney disease

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

Therefore, osteodystrophy, neuropathy, bilateral kidneys showed little abdominal ultrasonography, and anemia are typical initial results suggest that a chronic course of a singlenewly diagnosed with kidney failure in the absence of the basis of elevated BUN and serum creatinine.

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

Although acute lesions in the kidneycauses of death and detachment of tubular epithelial cells, often followed by regeneration, with restoration of regular architecture, the results provide continuous irreversible loss of nephrons. As a result, more weight is supported by fewer nephrons practices, which manifests as an improvement in glomerular filtration pressure and hyperfiltration.

For factors not well understood, this compensation hyperfiltration, which can be thought of as a form of "high" ofnephron level of the person, predisposes to fibrosis and scarring (glomerular sclerosis). As a result, the rate of destruction of nephrons and reduced increases, thus accelerating the progression of uremia, the complex of symptoms and signs that occurs when the residual renal target is insufficient.

Thanks to the extraordinary reserve of the kidneys practice, up to 50% of the nephrons can be lost with the evidence of short-term functional impairment. So people with twoHealthy kidneys are able to donate one for the transplant. When GFR is reduced even more, leaving only 20% of the initial renal capacity, some degree of azotemia (increased blood vessels of the products normally excreted by the kidneys) shows.

However, patients may be largely asymptomatic, simply because a new equilibrium is reached in the blood vessels levels of these products are no longer sufficient to cause overt toxicity. However, even in thisapparently stable level of evolution of renal hyperfiltration to accelerate end-stage chronic renal failure in progress.

Moreover, simply because people with this level of reserves TFG small practice, you can easily become uremic with any additional power (eg, viruses, obstruction, dehydration, or nephrotoxic drugs) or any other state catabolic in connection with a higher turnover of nitrogen - containing products with reduced GFR.

Thepathogenesis of renal failure resulting in ongoing part of the poisonous mix of results (1) stored products normally excreted by the kidneys (eg, nitrogen containing elements of the process of protein metabolism), (2) the regular products, such as hormones already present in abundance, and (3) the lack of normal kidney products (eg, loss of erythropoietin).

Results failure excretory fluid shifts, an increase of intracellular Na + and water and decreasingIntracellular K +. These alterations may contribute to the purpose of subtle alterations in 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 renal excretion of salt and water.

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

A recommendation for the typical patient with renal failure continues to avoid excessive salt intake and limiting fluid intake to make sure it is equal to the production of urine and 500 ml (insensible losses). Other adjustments to the standard can be done either through the use of diuretics (in a patient who otherwise makes the urine) ordialysis.

Why do these people also have impaired renal salt and water conservation mechanisms, are much more sensitive than normal to + sudden extrarenal sodium and water loss (eg, vomiting, diarrhea, increased sweating and fever). In these circumstances, much easier to create low ECF, the deterioration of renal ulterior motives (which may not be reversible), and vascular collapse or even shock.

Symptoms and indicators of dry mucous membranes,dizziness, syncope, tachycardia, decreased filling of the jugular vein, suggesting that the increase in the amount of exhaustion. Hyperkalemia is a serious problem in chronic renal failure, especially for those whose GFR fell below 5 ml / min. Above that level, such as falling glomerular filtration rate, aldosterone-mediated increase in K + transport in the distal tubule in the form of compensation.

Therefore, a patient with a GFR 50 ml / min and 5 ml / min in tubular transport function to maintain the balance of K +.Treatment with K +-sparing diuretics, ACE inhibitors or blockers, drugs that can alter the aldosterone-mediated K + transport can therefore precipitate hyperkalemia dangerous for people with chronic renal failure.

People with diabetes mellitus (the main trigger for the permanent kidney failure) may have a hyporeninemic hypoaldosteronism syndrome. This syndrome is actually 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, individuals are able to offset the decline in GFR, improving their aldosterone-mediated K + transport and therefore have relative difficulty of K + handling. This difficulty is usually manifested as hyperkalemia even before the GFR has fallen below 5 ml / min.

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

The reduced ability to excrete acid and base results in continuous renal generate no metabolic acidosis. In most cases, when the GFR is above 20 ml / min, acidosis develops only a reasonable time before the re-establishment of a new steady state production and use of the buffer.The decrease in pH of the blood vessels in these individuals can usually be corrected with 20-30 mmol (2.3 g) of sodium bicarbonate orally every day.

However, these people are extremely sensitive to acidosis in the case of a sudden acid load or the appearance of problems to improve the acid load generated. Several problems of phosphate, Ca2 + metabolic process, and the bone can be seen in permanent kidney failure as a result of a complex series of events.

Key factorspathogenesis of these problems include (1) a decreased uptake of Ca2 + in the intestine, (some) overproduction of parathyroid hormone (three), disordered vitamin D metabolism, and (4) chronic metabolic acidosis. All these factors contribute to increased bone resorption.

Hypophosphatemia and hypermagnesemia can occur through excessive use of phosphate binders and antacids containing magnesium, although hyperphosphatemia is more typical. Hyperphosphataemia contributes to improvinghypocalcemia and thus serves as a trigger for additional secondary hyperparathyroidism, elevated PTH levels in the blood.

Vessels from the high PTH blood bones further reduced Ca 2 +, and contributes to the lack of chronic renal osteomalacia (see discussion below). Congestive heart failure and pulmonary edema may develop in the context of the amount of salt and overload.

Hypertension is a typical finding of chronic kidney failure, also, in general, based on fluid and Na + overload. However,hyperreninemia is also a recognized syndrome in which renal perfusion falls triggers excessive production of renal renin and therefore do not raise systemic blood pressure.

Pericarditis result of irritation and inflammation of the pericardium by uremic toxins is a complication whose incidence continues to kidney failure is decreasing due to the first institution of renal dialysis. Increased cardiovascular risk is a complication seen in patients with chronic renal failure and remainstrigger death in this population.

It is the result of a myocardial infarction, stroke and peripheral vascular disease. Cardiovascular risk factors in these patients are hypertension, hyperlipidemia, glucose intolerance, increased heart valve calcification and chronic myocardial ischemia is a consequence of increased Ca2 + x PO43 product as well as other less well characterized uremic middle .

People with permanent kidney failuremarked abnormalities in red blood cells, white cells and clotting parameters purpose vessels. Normochromic, normocytic anemia, with signs and symptoms of apathy and fatigue easily and usually hematocrit levels 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 failure, dialysis, regardless of location, show aa significant improvement in hematocrit during therapy with erythropoietin (epoetin alfa).

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

People with chronic renal failure show abnormal haemostasisshows the highest reduction of bruises, the increase in surgery of blood vessels, and a high incidence of spontaneous gastrointestinal hemorrhage and stroke (including hemorrhagic stroke and subdural hematomas).

Laboratory abnormalities include prolonged bleeding time, decreased platelet factor III, platelet aggregation and adhesion abnormal prothrombin and the use of altered, this is not fully reversible, even in patients on dialysis as well. Uremia is associated with highsusceptibility to infections, considered by the removal of leukocytes from uremic toxins.

The repression appears to be greater for neutrophils and lymphoid cells also appear to affect the chemotaxis, the acute inflammatory response, delayed hypersensitivity and leukocyte functions more than others. Acidosis, hyperglycemia, hyperosmolarity, and malnutrition are also thought to contribute to immunosuppression in renal continuum.

The invasive nature of dialysisand the use of immunosuppressive drugs in patients undergoing kidney transplantation also contribute to an increased incidence of infections. Signs and symptoms of CNS and the variety of indicators could sleep disorders and mild impairment of mental concentration, poor memory, misconceptions, and neuromuscular irritability (manifested as hiccups, cramps, twitches and spasms) of asterixis, myoclonus, stupor, convulsions and coma in terminal uremia.

Asterixis is manifested in involuntarybeat movement is seen when the arms are extended and wrists restricted to "stop the visitors." E 'due to the damaged nerve conduction in the wide range of metabolic encephalopathy causes, including renal failure.

Peripheral neuropathy (upper and lower extremity sensory and motor high), which is characterized by restless legs syndrome (localized sense some discomfort and involuntary movements of the lower limbs), is a frequent finding in continuous renalfailure and an important signal for the start of dialysis.

Patients on hemodialysis may develop aluminum toxicity, characterized by the word dyspraxia (inability to repeat words), myoclonus, dementia and seizures. Similarly, aggressive acute dialysis imbalance can result in a syndrome characterized by nausea, vomiting, drowsiness, headache, seizures, and within an individual with a much larger roll.

Presumably, this really is an impact of rapid change in pH or osmolalityin the extracellular fluid, causing cerebral edema. GI nonspecific findings in uremic patients include anorexia, hiccups, nausea, vomiting, and diverticulosis. Although its pathogenesis is not obvious, many of these outcomes improve with dialysis. Lord with uremia have reduced amounts of estrogen, which perhaps explains the high incidence of amenorrhea and the observation that almost never are able to carry a pregnancy to term.

Regular periods, but a higher rate of productivitypregnancy usually return with frequent dialysis. Similarly, low testosterone levels, impotence, oligospermia, and germinal cell dysplasia are common findings in men with permanent kidney failure. 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 patients with diabetes whose blood glucose was previously difficult to control. Skin markings are derived from numerousthe results of continuous renal currently under discussion.

Renal failure patients may appear pale due to continuous changes in anemia, accumulation of metabolites on the color or gray pigment as a result of transfusion-mediated hemochromatosis, bruising and hematomas as a result of bleeding disorders, and pruritus and excoriations be the result of Ca2 + deposits of secondary hyperparathyroidism. Finally, when the concentrations of urea arehigher sweat evaporation leaves a residue of urea called "uremic frost".