Increased soluie delivery to the macula densa, stlmulating anglotensin release from Juxtaglomerular cells

In Increased soluie delivery to the macula densa, stlmulating anglotensin release from Juxtaglomerular cells (c) More severe tubular damage causes reduction in tubular flow thus predsposing to intraluminal tubular obstruction. Sparing of some tubules may be the explanation for non-oliguric acute tubular necrosis (d) In ATM- apart from tubular damage, some toxins may impair glomerular permeability damaging endothelial or rnasangial cells, or indirectly by affecting glomerular blood flow. Clinical features - Stages -1 EARLY OR PPE-OLIGURIC STAGE - This is overshadowed by symptorrs of the primary cause Symptoms like lethargy , nausea, headache, are incfcative overhydration and should arouse suspicion of impending renal Insufficiency Characteristics are lack of structural damage, retention of the ability to concentrate urine and rapid reversibility if circulatory Insufficiency is corrected promptly and completely. 2. OLIQURIC STAGE -1 2. (a) oligurla - less than 400 ml urine In 24 hours in adults) sets In majority within 24-48 hours The duration varies, average being 4-10 days. Complete anuria is rare and indicates either a severe renal catastrophe or obstructive etiology (b) Gastrointestinal -Anorexia, nausea, vomiting, at times diarrhoea, mouth ulceration. Adynarric ileus or pseudo-paritonitis if these are related to uncontrolled uremia, they dsappear after dialysis (c) Circulatory -Hypertension is common in acute glomerulonephritis, renal infarct and cortical necrosis and when ARF results from intoxication by organic solvents Severe hypertension Is usual in malignant nephrosclerosis or thrombotic rrilcroanglopathy Pericardtis is uncommon, (d) Respiratory Dyspnoea is related to metabolic acidosis, to pulmonary infection or oedema