Renal and Acid-Base Physiology

Good glycemic control appears to be of benefit in slowing the rate of renal progression. The outcome from transplantation is better for non-diabetic patients than for diabetic patients. Transplantation prolongs life expectancy in diabetic patients with end stage renal disease.

Focal segmental glomerulosclerosis has a poor prognosis and is associated with HIV infection.

Potassium secretion occurs only from the principal cells of collecting duct and it is this potassium secretion that is used to control potassium.

RAST testing is not helpful as most patients are atopic and therefore, react to many environmental allergens. There is a better correlation of clinical relevant allergen with skin prick testing. This is used routinely, particularly in adults. 

All the glomeruli are in the renal cortex. The loop of Henle dips into the medulla and the collecting ducts drain into the renal pelvis by passing through the medulla.

There are osmoreceptors in the hypothalamus that detect an increase in plasma osmolality. In response to input from these receptors and other stimuli, cells in the posterior pituitary gland release ADH.

The common causes of urinary tract infection are Escherichia coli, Klebsiella and Proteus species. Staphylococci are not the common cause of urinary tract infection.

Aldosterone excess causes excess renal bicarbonate reabsorption.

It is produced by plasma cells and B cells in the usual way.

Cholesterol and lipids in skin modify the antigenicity of streptolysin O and suppress the ASO antibody response, but not the anti-DNAse B antibody titre.

Renal tubular acidosis occurs when kidneys do not adequately reabsorb bicarbonate.

Asthma is a chronic lung disease that inflames and narrows the airways.

Prostaglandins are powerful vasodilators and there is a normal tonic level of vasodilation in the renal blood vessels. It is caused by prostaglandins.

Insulin causes potassium entry into cells. It is used in the emergency treatment of severe hyperkalaemia. As insulin also causes a fall in blood glucose levels, exogenous glucose is usually given with the insulin to prevent this.

Excess parathyroid hormone raises plasma calcium levels. In primary hyper parathyroidism, there is a primary increase in parathyroid hormone and so, a rise in plasma calcium. Too much PTH raises the levels of calcium in the blood.

This histological term means an increase in the number of cells within the glomerular tuft.

The osmolality of filtered fluid entering the proximal tubule from the glomerulus is essentially that of plasma from which it is produced. Reabsorption in the proximal tubule is iso-osmotic. It means that the osmolality of the tubular fluid does not change because solutes and water is removed together in the same ratio at which they are present in the tubules. For this reason, the concentration of urine (i.e. its osmolality) in the proximal tubule is not altered.

The basic problem is usually loss of water. It is treated with careful replacement of water. As with hyponatremia, it is important not to replace the loss too quickly. The cells make compensatory changes during hyperosmolar conditions and a sudden change can be dangerous as the cells do not have time to readjust back to normal. The best way to prevent this is to keep checking the plasma sodium to ensure that it is not changing too quickly.

It is the disease which is limited to children and accounts for 90% cases of nephrotic syndrome.

Spironolactone opposes the actions of aldosterone. It has the opposite effect. It is an aldosterone receptor antagonist that causes kidneys to remove water and sodium from the body, with reduced losses of potassium.