Posts Tagged ‘acute reanl failure’

Bio-chemical diagnosis of cardiac injury or infarction is  well  documented modality for many decades. Now , acute coronary  syndrome is diagnosed  by a battery of tests  that  detects the  proteins leaking from the  injured  myocardium.

Nephrologists have long been aiming for  such a  marker for ischemic  renal injury  (Not withstanding the fact , they are already blessed with two age-old molecules  creatinine and BUN !)

Neutrophil gelatinase associated Lipocalin (NGAL)

  • This is 25 Dalton molecule  richly secreted within renal  cortical cells in response to ischemic injury .
  • It is released without  modification in the  urine  .High urinary levels  of NGAL  reflect  acute renal  injury.
  • Early experience shows it  is a  promising  investigation and could  become a regular biochemical test in the near future.
  • Urine level of  NGAL >250 ng/ml , 2 hours   after cardiac surgery  predicts impending renal failure  in the next 24-48 hours .The advantage is , it NGAL raises well before serum creatinine.

NGAL After cardiac surgery


Lipocalin following PCI

Bachorzewska-Gajewska H et al. Neutrophil-gelatinase-associated lipocalin and renal function after percutaneous coronary interventions. Am J Nephrol 2006; 26: 287-292.


References for  NGAL


Final message

  • Cardiologists  and cardiac surgeons  have started  performing  complex    PCIs and  CABGs in  patients with   delicately  and precariously balanced renal function.
  • While ,  cardiologists   challenge  the kidneys with high  osmolar contrast agents ,  the surgeons stress it with extra corporeal circulation.  Many of these patients also  have co- morbid conditions .
  • Often , the cardiac outcome is directly linked to pre /post procedural  renal function .Nephrologists usually  arrive  late  into the filed (Creatinine SOS calls !).By this time the full-blown ATN sets in many.

Now , we have a tool to identify impending ARF , it gives us  little more time and  flexibility in managing the issue .

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It is traditionally believed  , renal blood flow is critically determined by the  luminal diameter  of  renal artery.But in reality  there are more important factors  other than renal  arterial diameter  that determine the glomerular  blood flow.  As in any vascular bed, it is the arterioles that determine the resistance and hence the flow . These arterioles  form the  critical  resistance  points and acts as   check  valves in this  “vascular  highway”  flowing across the renal terrain !

Unlike other micro-circulations ,  the kidney has a  special job to do ,  ie  filtering  the toxic  molecules.  Hence,   for the blood entering the kidneys  , even  nourishing the kidney seems ,  a less important  function !  The nephrons  of the kidneys are probably the most  “high – tech” cells in human body (Of course ,next only to brain cells ) .The vascular  tuft of glomerulus located within the bowman’s capsule  is perfused  by afferent arteriole and drained by efferent arteriole .

The entry of blood into glomerulus is regulated both by afferent and  efferent arteriolar  tone .These  two micro-circulaoty units  are under the  sensitive control of both neural  and humoral  signals. Glomerular circulation is meticulously  regulated by renal juxta glomerular apparatus.It modulates the glomerular  blood flow by secreting renin which  acts through Anigiotensin 2  on the   efferent arteriole .

The tone of the  efferent  arteriole  is thought to be the single important factor in this servo control mechanism.

What happens in bilateral renal arterial stenosis ?

When there is bilateral renal arterial stenosis the effective renal blood flow is not  significantly reduced , but maintained at  the cost of increasing the efferent arteriolar constrictor tone. It  is  like a  check valve at  the  exit point of a dam , which is partially closed to maintain the adequate pressure head (Here , intra-glomerular  pressure head )

What happens when ACEI are introduced ?

Once ACE inhibitor  is administered , the efferent arteriolar   tone is removed , this triggers  the intra glomerular pressure to drop  suddenly and filtration pressure reduces .

Note: ACEI does  not reduce the renal  blood flow  directly  but  the glomerular  perfusion pressure drops hence precipitating acute renal function deterioration.

What is your comment about the reno-protective effects of ACEI ?

The medical science’s  most  crucial  moments  occur  , when we confront  two diagonally opposite views  are  debated  and both  suggest , there is definite benefit for the patient ! Cardiologists and nephrologists were always  made to believe  ,  ACEI are  unfriendly to kidneys . But ,we now have  evidence , ACEI is not an untouchable molecule in renal  dysfunction.

This is based on  the observations made , over the years that  excess Angiotensin 2  is  ultimately a liability for the kidneys !

Looking at a  long  term perspective  , AT 2  increases the intra -glomerular hypertension and ACEI inhibitors reduce it.This  pr0tects the  nephrons from  hyper-filtration  mode ,  that accelerates the  glomerular  injury . So , the  current thinking  is  ACEI has a definite role in arresting the progress of  renal cell injury .

This is akin to beta blocker story in CHF which was initially contraindicated in CHF later became a definite indication

The only issue for ACEI is , it should not be continued if an ARF like picture sets in .(Acute deterioration ). Otherwise ,  in CRF at any  basal level of serum creatinine  , ACEI can be continued . Some think even an  increase by few mg of creatinine  can be allowed .

So the following can be a working guideline *

  • ACEI can be started  or continued at any level of creatinine in stable CKD with or without dialysis

But ,ACEIs need to be stopped in all of the following 

  • Acute renal failures
  • Acute on chronic renal  failure
  • Accelerated elevation of  creatinine  (As in bilateral renal artery stenosis)

How much elevation of creatinine is allowed in CKD  with ACEI  ?

This is   not answered yet .

*Caution : The above conclusions on ACEI and creatinine was  derived  by me , based on  with  personal discussions with my  Nephrology colleagues. It may  be subjected to correction.


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