Question

Explain the pathophysiology of acute renal failure in a patient who is suffering from severe haemorrhage resulting from a motor vehicle accident.

Answer 1

Ans.

pathophysiology of acute renal failure -

Acute kidney injury (AKI) is the leading cause of nephrology consultation and is associated with high mortality rates. The primary causes of AKI include ischemia, hypoxia or nephrotoxicity. An underlying feature is a rapid decline in GFR usually associated with decreases in renal blood flow.

Pathophysiology

In view of the different clinical presentations, ARF in the NS is not a single, uniform pathophysiological entity. Factors that can be singled out to contribute to the decrease in glomerular filtration rate (GFR) are a low renal perfusion pressure, a decreased filtration coefficient, high intratubular pressure, ATN, interstitial nephritis and interstitial oedema.

In the case of overt hypotension, a pre‐renal cause can be suspected. This is encountered particularly in children with persistent proteinuria that is so severe that blood volume cannot be maintained, such as in congenital NS. In children with relapsing minimal lesion NS, hypovolemic ARF may be encountered early during a relapse. The acute start of heavy proteinuria probably causes a disequilibrium between plasma and interstitial albumin concentrations. However, when plasma protein drops, proteinuria diminishes, and is often insufficient to remain a threat for hypovolemia as in congenital NS. We have tried to amend this in children presenting with early relapse of minimal lesion NS [8]. Half of them had ‘hypovolemic symptoms’. Compared with non‐symptomatic children, they had stimulated neurohumoral factors and strong tubular sodium reabsorption, and a suppressed urinary dilution capacity, compatible with the presence of a pre‐renal factor. However, even in these children renal plasma flow was high, and the decreased GFR thus reflected a decreased filtration fraction.

In adults, proteinuria is generally not marked enough to endanger the circulation [9]. Relapses of minimal lesion NS develop more slowly, but may occasionally be acute, as occurs in children. It cannot be excluded, however, that adults with established NS are more liable to develop ARF if they suffer from some other complications such as septicaemia or blood loss. Indeed, blood volume that is normal while recumbent may drop below normal when standing. On the other hand, mobilization of excess tissue fluid in hypoproteinemic conditions is highly efficient [9]. Excess fluid can mostly be removed without inducing hypotension or renal failure. However, complete removal of excess fluid may create an unsteady condition were changes in blood volume cannot be compensated.

Approximately 30% of children [10] and adults [11] with idiopatic NS have a significant decrease in GFR. This is due to an intrinsic filtration impairment, since filtration fraction is low. Conceivably, ARF may reflect worsening of this intrinsic problem. However, glomerular changes, i.e. obliteration of epithelial slit pores as visible with electron microscopy, are not correlated with the reduction in GFR in humans. Filtration can also be impaired by a high intratubular pressure caused by protein casts [1,2], but this possibility has received little attention. The following case history illustrates the possible importance of this factor