Potassium and acid base

Hypokalemia is associated with alkalosis and Hyperkalemia is associated with acidosis! We have heard about this but did ‘t know if this had mechanistic/pathogenetic significance until we heard Dr.Weiner’s lecture today.

Hypokalemia increases ammonia production in proximal tubule which is absorbed into the interstitium in the ascending loop of Henle through NKCl cotransporter (since the concentration of ammonia is several hundred folds higher than potassium in hypokalemic state). The ammonia  decreases the activity of ENaC in the principal cell , which decreases potassium excretion(this is favourable in hypokaleic state since K is conserved by this) and ammonia combines with proton secreted in the alpha intercalating cell thereby increasing net acid excretion.

In short, hypokalemia signals the cortical collecting duct to decrease potassium excretion by increasing the production of ammonia.

Hyperkalemia decreases ammonia production in proximal tubule and the net acid excretion is decreased.

It was interesting to know the cause of hyperkalemia in acidosis!

This explanation based on ammonia generation hypothesis holds good only in chronic acidosis and not in acute acidosis such as DKA and lactic acidosis.


Water diuresis and osmotic diuresis

Both water diuresis and osmotic diuresis can lead to hypernatremia!  How do we differentiate?


Water diuresis and osmotic diuresis , both present with hypernatremia and polyuria!

In water diuresis, the osmolar excretion per day is less than 1000 mOsm/day (calculated from urine osmolar concentration and urine volume) and in osmotic diuresis, the osmolar excretion per day is>1000   mOsm/day.

Water diuresis occurs in Diabetes insipidus

Osmotic diuresis occurs in Parenteral nutrition with heavy protein intake(10 grams protein yield 50 mOsm of urea) and  Diabetes mellitus(glucose is the osmole in urine that drags water with it)

It is nice to understand this concept. However in clinical situation the numbers don’t matter so much and the free water loss  is usually  from a combination of several factors!

Like,  Critically ill intubated patient recovering from ATN on TPN for nutrition. Here you have no access to free water, water diuresis from recovering ATN(some degree of renal concentrating defect/nephrogenic DI) and osmotic diuresis from TPN!

Nevertheless, it helps us identify the major contributor !