Clinical Effects of Chronic Renal Failure (CRF)

Clinical Effects of Chronic Renal Failure (CRF)

The kidneys are able to maintain the chemical composition of fluids within normal limits until more than 50% of functional renal capacity is destroyed by diseases or injury. Chronic renal insufficiency or failure begins when the diseased kidneys can no longer maintain normal chemical structure of body fluids under normal conditions. Progressive deterioration over months or years produces a variety of clinical syndrome known as Uremia. The pattern of renal dysfunction is remarkably uniform no matter what disease process initiates the advanced disease. Renal vascular disorders such as hemolytic-Uremic syndrome, vascular thrombosis, or cortical necrosis are less frequent causes.

Diagnostic criteria

1. Clinical

• Tiredness, fatigue, headache, loss of appetite, vomiting,

• PolyUria, nicturia, polydypsia, bone and joint pains, retardation of growth, dryness and itching of skin

• Muscular convulsions, paresthesias, signs of sensor or motor neuropathy

• Heart failure and hemodynamic disorders

2. Laboratory;

• Decrease of glomerular filtration rate

• Metabolic acidosis

• Anemia

• Decrease of thrombocytes’ adhesion

• Heperkalemia, hyperphosphatemia, hypocalcemia, hypoproteinemia, hyperuricemia

• Isostenuria

• Renal osteordystrophy

• X-ray examination of the chest may reveal cardiomegaly, hypertrophy of the left ventricle, aortectasia, lung’s edema, pleural exudates.

Causes of chronic renal failure

1. (a) Glomerular diseases

• Of unknown etiology

• Associated wirh systemic lupus erythematosus (SLE), poly-arteritis nodosa

• Henoch-schonlein vasculitis

(b) Familial nephropathy

• Nephronophthisis

• Alport’s syndrome

(c) Hemolytic Uremic syndrome

(d) Amyloidosis

2. Congenital anomalies

• Bilateral renal dysplasia

• Congenital nephritic syndrome

• Polycystic kidney

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Clinical manifestations

The first evidence of difficulty is usually loss of normal energy and increased fatigue on exertion. For example, the child may prefer quiet, passive activities rather than participation in more active games and outdoor play. The child is usually somewhat pale, but it is often so inconspicuous that the change may not be evident to parents or others. Sometimes the blood pressure is elevated. As the disease progresses, other manifestations may appear. The child eats less well (especially breakfast), shows less interest in normal activities, such as schoolwork or play, and has an increased urinary output and a compensatory intake of fluid. For example, a previously dry child may wet the bed at night. Pallor becomes more evident as the skin develops a characteristic sallow, muddy appearance as the result of anemia and deposition of Urochrome pigment in the skin. The child may complain of headache, muscle cramps, and nausea, Other signs and symptoms include weight loss, facial puffiness, malaise, bone of joint pain, growth retardation, dryness or itching of the skin, bruised skin, and sometimes sensory or motor loss. Amenorrhea is common in adolescent girls.

The therapy is generally instigated before the appearance of the Uremic syndrome, although there are occasions in which the symptoms may be observed. Manifestations of untreated Uremia reflect the progressive nature of the hemeostatic disturbances and general toxicity. Gastrointestinal symptoms include anorexia and nausea and vomiting. Bleeding tendencies are apparent in bruises, bloody diarrheal stools, stomatitis and bleeding from lips and mouth. There is intractable itching, probably related to hyperparathyroidism, and deposits of Urea crystals appear on the skin as “Uremic frost”/ There may be an unpleasant “Uremic” odor to the breath. Respiratons become deeper as a result of metabolic acidosis, and circulatory overload is manifest by hypertension, congestive heart failure, and pulmonary edema. Neurologic involvement is reflected by progressive confusion, dulling of sensorium, and, ultimately, coma. Other signs may include tremors, muscular twitching and seizures.

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