Acute Kidney Injury

Acute kidney injury (formerly known as acute renal failure) is defined as a syndrome arising from a rapid fall in GFR over hours to days. The criteria used is either urine output or serum creatinine.AKI may be staged from stage 1 to stage 3.Such staging is more for epidemiology than of any clinical significance.

Classification- AKI may be classified as prerenal ARF, ATN (acute tubular necrosis),intrinsic renal disease, post renal or obstructive uropathy.

Prerenal ARF is due to reduced renal perfusion causing a reduced GFR.It is important to understand that hypoperfusion is not equivalent to volume depletion. It is the effective arterial blood volume(EABV) that matters.EABV may be considered as analogous to BP which is a product of cardiac output and total peripheral vascular resistance.Thereforehypovolaemia indeed will lower the EABV.Causes of hypovolaemia are haemorrhage, severe vomiting, diarrhoea, burns, salt loosing nephritis and diureticoverusage.Reduced peripheral resistance which results from vasodilation causing an increased vascular capacitance as occurs in septic shock, anaphylaxis and hepatorenalsyndrome will cause a drop in EABV and renal hypoperfusion.Cardiac failure will cause a reduction in cardiac output and drop in systemic BP which compromises renal perfusion.

Intrinsic renal disease are caused by:-

1. Glomerulonephritis
2. Interstitial nephritis usually drug induced
3. vasculitis like SLE, polyarterits nodosa, wegenersgranulomatosis

ATN and prerenal ARF are just on opposite ends of a continuum of renal damage. All that causes prerenal ARF may cause ATN. Postrenal ARF or obstructive uropathy may occur from bladder outlet obstruction like prostrate hypertrophy or bilateral ureteric obstruction from renal calculi or malignant infiltration. Clinical approach to AKI. It is important to recognise the at risk groups of patients who are:-

1. Elderly patients
2. DM with established diabetic nephropathy
3. Patients on ARB, ACEI, NSAID.
4. Hypovolaemia
5. Multiple myeloma
6. Patients undergoing surgeries especially hepatobiliary, cardiac and vascular surgery like repair of abdominal aneurysm.

History taking must include drug history like NSAID, alternative or herbal medication, history of pre-existing renal disease like diabetic nephropathy. All medications that patient is on must be noted. Clinical evaluation of fluid status is important. Never miss a distended bladder. The most discerning indicator of hypovolaemia is a postural drop of 20 mmHg systolic pressure. One must not be rigid over the 20 mm figure. I have seen a patient who presented with typical complain of giddiness on getting up from bed. His postural drop was only 10 mm Hg.In this context, I am sure the 10 mm Hg is significant. Incidentally he was started on lasix 40 mg daily,micardis 40mg daily and coralan 5 mg daily about a month by his cardiologist. Blood must be sent for renal profile, full blood count, LFT, calcium, phosphate, uric acid andUFEME.Collagen screening and vasculitic screen like anti DsDNA, ANCA Ab,Anti GBM are not routine and only done on suspicion like active urinary sediments of proteinuria, haematuria and casts. During our undergraduate days, we were taught that analysing the urine for sodium concentration, osmolarity,urine/plasma creatinine ratio will determine if it is prerenal ARF or ATN.I personally never bother, because it does not assist in management. Attempt to do so will most likely result in conflicting figures. Because in reality, there is never a 100%prerenal ARF or a 100% ATN.Most are in between. Retrospectively if renal function returns after correction of hypovolaemia, it is prerenal ARF, if not it is established ATN.

A renal and bladder ultrasound is certainly advised as it is easily available and easy to do. It helps to rule out obstruction (Acute obstruction may not give hydronephrosis).A small and echogenic kidney indicate underlying chronic renal failure. Normal kidneys mean nothing.

I would put in a CBD to monitor strict I/O chart. The most important initial management is to correct hypovolaemia.For patients who are difficult to clinically judge volume status like elderly patients, haemodynamically unstable with hypotension and those whom I anticipate will need dialysis, I would promptly insert a triple lumened internal jugular catheter under ultrasound guidance. Boluses of fluid, 200 ml of N/SALINE would be a good choice is given. After every infusion, CVP is checked and patient clinically assessed. Once euvolaemia is achieved, a bolus of IV frusemide 80 mg is given to promote diuresis.Return of diuresis do not always mean recovery, it may just convert anoliguric ARF to a nonoliguric ARF which is much easier to handle. Fluid maintainanceamounts to urine output daily plus 500 ml insensible loss daily. Meanwhile all nephrotoxic drugs like ACEI, ARB, NSAID and aminoglycosides are omitted. If after rehydration, BP remains low as in cardiac failure or SIRS (systemic inflammatory response syndroms) from sepsis or pancreatitis etc, inotropic support is required. Such cases carry a high mortality as it indicates multiorgan failure.

When to refer to a nephrologist-

1. When the need for dialysis is imminent like severe acidosis PH<7.0, pulmonary oedema, hyperkalaemia, severe uraemia which is left to the discretion of the attending doctor to decide.
2. Suspicion of an underlying glomerulonephritis or vasculitis like active urinary sediments. Prompt treatment with steroids and immunosuppressive agent may abort a catastrophic rapidly progressive or crescenteric glomerulonephrits with irreversible loss of kidney function.