This Renal Failure Index (RFI) calculator for acute tubular necrosis evaluates the prerenal or renal cause of acute renal failure and helps monitor creatinine levels. Below the form you can read more about all the causes involved in ATN.

Urine sodium:*
Serum Creatinine:*
Urine Creatinine:*

How does this Renal Failure Index (RFI) calculator for acute tubular necrosis work?

This is a health tool that determines the RFI value in patients who are suspect of acute kidney failure due to acute tubular necrosis.

This Renal Failure Index (RFI) calculator provides three fields to input the clinical determinations required, one measured in mEq/L and the other two measured in mg/dL as explained below:

■ Urine sodium – measured in miliEquivalents per dL. With a normal low of 25 and a normal high of 150 mEq/dL.

■ Serum Creatinine – breakdown product in the metabolism of the muscles and certain tissues, filtered by the glomerulus, with a normal range between 0.6 and 1.3 mg/dL.

■ Urine Creatinine – creatinine levels that escape the filtration process and are excreted through urine, normal range between 40 – 120 mg/dL.

Increased creatinine levels are indicative of:

■ Impaired renal function;

■ High protein diet;

■ Use of anabolic steroids;

■ Rhabdomyolysis.

Renal failure index

This is a renal function test aimed at assessing the function of the kidneys and at revealing whether the cause of acute failure is renal or prerenal:

■ RFI > 1 indicates renal causes;

■ RFI ≤ 1 indicates prerenal causes.

By differentiating between prerenal azotemia and oliguric acute renal failure, this index is used in the first stages of diagnosis alongside other clinical determinations.

The main areas of focus within renal function tests include BUN (blood urea nitrogen), Creatinine, fractional excretion of sodium / urea and uric acid.

The following is a list with the most common risk factors for kidney disease:

■ Older age, family history of CKD;

■ Decreased renal mass;

■ Diabetes mellitus;

■ Hypertension;

■ Systemic infections;

■ Urinary tract infections (UTI);

■ Nephrolihiasis;

■ Autoimmune disease.

Acute Renal Failure (ARF) and Acute Tubular Necrosis (ATN)

Beside the index result discussed above, there are clinical findings that suggest either the prerenal (volume depletion, existing CHF - congestive heart failure, severe liver disease, edema) or the postrenal causes (palpable bladder, hydronephrotic kidneys, enlarged prostate, renal calculi).

ARF is characterized by azotemia, supported or not by oliguria and that progresses in a matter of hours or days.

Early recognition of the causes of ARF is essential in the quick initiation of treatment as this is a condition often affecting hospitalized patients and carries high morbidity and mortality rates.

There is a classification of the severity and changes in serum creatinine or urine output are monitored to check the entry criteria for RIFLE:

■ Risk of renal dysfunction;

■ Injury to the kidney;

■ Failure of kidney function;

■ Loss of kidney function;

■ End-stage kidney disease.

ATN – acute tubular necrosis is characterized by modifications appearing in the tubular epithelial cells and is the most common cause of AKI (Acute Kidney Injury). Most likely, the mechanism is started by low blood pressure and/ or use of nephrotoxic drugs. Urinalysis shows epithelial cells in urine and this is the main diagnosis modality.

ATN is either classed as toxic or ischemic, depending on the agent that started the depletion of the epithelial cells, exposure to toxic substances or lack of oxygen from the capillaries.

Toxic acute tubular necrosis is either caused by free hemoglobin, some antibiotic use, statin use or by cytoxic drugs.

Ischemic ATN occurs due to insufficient perfusion like in renal artery stenosis, embolism or shock.


1) Miller TR, Anderson RJ, Linas SL, Henrich WL, Berns AS, Gabow PA, Schrier RW. (1978) . Ann Intern Med; 89(1):47-50.

2)Durakovic Z, Durakovic A, Durakovic S. (1989-1990) . Ren Fail; 11(4):213-9.

3) Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P. (2004) . Crit Care; 8:(4) R204-12.

01 Nov, 2015 | 0 comments

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