As I promised recently, we'll take a brief look at the biochemical changes that occur in renal failure. This is not a post about the pathophysiology of renal failure - that will have to wait. Rather, this is an aid to understanding why, for instance, sodium often decreases when the kidneys start shutting down.
Firstly, what are the typical biochemical changes that accompany renal failure? Basically, they are summarised by this table, adapted from William J Marshall's Clinical Chemistry (4th edn.):
Ok, now for the why.
If our kidneys shut down suddenly, what would happen to the the concentrations of the blood's various ions? Surely the blood level of those things that the kidney normally excretes would go up? Largely, this is the case, and this decreased excretion explanation holds true in many cases. But as the table shows, there are exceptions. Let's break them down one by one...
- Potassium - the rise is due to (1) decreased excretion and (2) intracellular displacement of potassium by the increased hydrogen ions, leading to a rise in the extracellular potassium level. Also, in many cases the renal failure coexists with a state of marked tissue breakdown (e.g. crush injuries, systemic hypoperfusion), and so the serum potassium will rise as potassium leaks out of the damaged cells.
- Sodium - sodium may be normal, although it is common for it to be decreased. Although less sodium is excreted than before, the water retention may outweigh this, causing the sodium level falls. The reasons for the excessive water include (1) excessive intake or excessive intravenous fluids and (2) increased water formation from oxidative metabolism (water is an obligate byproduct of this process, which is often increased in the states where renal failure coexists.)
- Phosphate - the rise is due to decreased excretion.
- Calcium - this has been covered in this post.
- Magnesium, urea and creatinine- also due to decreased excretion.
- Hydrogen ions - you probably already know that renal failure is an important cause of a metabolic acidosis. But why is this so. Firstly, (1) there is decreased excretion of the H+ load that the body produces. But it's worse than that. Adequate H+ excretion also requires urinary buffers, and the two main ones are phosphate and ammonia. But, recall, the amount of phosphate filtered is greatly reduced in renal failure. Thus, the urinary (as opposed to the plasma) phosphate level is markedly decreased, and the kidney is thus deprived of an important buffer. Its other major buffer - ammonia - is usually synthesised by the renal tubular cells, and this process is also obviously significantly thwarted in renal failure. (This bit may be a little obscure if you're new to urinary buffers and H+ homeostasis, but just leave a question in the comments section and I'll try to answer any queries about it.)
Are there other reasons behind the above biochemical changes? Do the reasons sometimes differ in acute vs chronic renal failure? Are there other ions worth mentioning? Yes, yes, and yes. But this is only meant to be a concise, understanding-based forum for medical queries, not a biochemistry textbook, so I've obviously had to leave bits out here and simplify a bit there. Feel free to leave comments though, if you feel I've misrepresented things in any way, and I'll do my best to rectify it.
Reference: "Clinical Chemistry" (4th edn.) - Marshall