Urine Formation

ADH prevents diuresis. It increases reabsorption of H20.

Presence of nitrite in urine indicates presence of bacteria in urine since some bacteria convert nitrate into nitrite in urine.

Acute tubular necrosis  is most commonly due to renal ischaemia, as in this case, though direct pharmacological toxicity can also be the cause among many others including haemorrhage, diuretics, contrast during radiological procedures and heart failure. The clinical course is dependent on the offending factor and degree of damage but most commonly early oliguria followed by recovery of renal function with an increase in renal output. GFR, however, may remain low due to tubular damage. Full renal capacity is usually regained within 6 weeks of the initial stressor. Haemolytic uraemic syndrome (HUS) (A) defines the acute injury to the kidney from RBC fragmentation which usually originates from thrombosis within arteries. HUS is therefore the triad of microangiopathic haemolysis, thrombocytopenia

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Urine volume can be as low as 0.5 L/day in a dehydrated person or as high as 20 L/day in a person who has been drinking tremendous amounts of water.

Specific gravity of urine is the measure of dissolved solutes (particles) in urine. It is low in diabetes insipidus and high in diabetes mellitus, acute renal failure and excess medications.

Benedict test is used to detect glucose which is reabsorbed in PCT.

Aquaporin-1 is localized to both the basolateral and apical membrane of the proximal tubules and its presence allows water to move rapidly out of the tubule along the osmotic gradients set up by active transport of solutes, and isotonicity is maintained. 60-70% of filtered water is reabsorbed in PCT.

Normally, GFR is about 180 L/day, and tubular reabsorption is 178.5 L/day, leaving 1.5 L/day of fluid to be excreted in the urine.

This patient is most likely suffering from analgesic nephropathy in view of the chronic history of NSAID consumption. Chronic intake can result in papillary necrosis and tubulointerstitial nephritis leading to anaemia, UTIs and haematuria. Diagnosis is made by ultrasound or CT scan alongside this clinical picture. An ultrasound is particularly useful if patients complain of sudden flank pain which can result from sloughed papillae causing urinary obstructions. Antegrade pyelography (D) is used to investigate a potential area of obstruction within the kidney which is not indicated in this case. Retrograde pyelography (A) is conducted to investigate obstructions via a catheter. A renal biopsy (B) would be useful to assess the degree of damage to the kidney but this is not essential as stopping analgesics or replacing them with alternatives, such as paracetamol, can reduce or even improve the condition. An abdominal x-ray alone would not be a useful modality for revealing renal damage in this case (C).

Orthotolidine test is used to detect blood in urine.

PCT has maximum capacity of reabsorption. Most of the reabsorption takes place here.

PCT has maximum capacity of reabsorption. Most of the reabsorption takes place here.

Thiazide diuretics have a unique effect on the distal tubule; they increase Ca2+ reabsorption, thereby decreasing Ca2+ excretion and clearance. Because parathyroid hormone (PTH) increases Ca2+ reabsorption, the lack of PTH will cause an increase in Ca2+ clearance. Furosemide inhibits Na+ reabsorption in the thick ascending limb, and extracellular fluid (ECF) volume expansion inhibits Na+ reabsorption in the proximal tubule. At these sites, Ca2+ reabsorption is linked to Na+ reabsorption, and Ca2+ clearance would be increased. Because Mg2+ competes with Ca2+ for reabsorption in the thick ascending limb, hypermagnesemia will cause increased Ca2+ clearance.

Aquaporin-1 is localized to both the basolateral and apical membrane of the proximal tubules and its presence allows water to move rapidly out of the tubule along the osmotic gradients set up by active transport of solutes, and isotonicity is maintained. 60-70% of filtered water is reabsorbed in PCT.

Glucose is completely reabsorbed by kidney unless any abnormality.

Factors regulating NaCl reabsorption from ALH:
1. It is increased by large NaCl load presented to ALH, sympathetic activity, angiotensin II & norepinephrine
2. It is decreased by prostaglandin & loop diuretics