Rahaf Wardeh Internal Medicine 2016 - 2017

Acute Renal Failure – Dr. Wael Omar (AQH)

Functions of the kidney:

Maintain: water balance, electrolyte balance, acid-base balance

Endocrine: secretion of erythropoietin, activation of vitamin D, Renin-Ang-Aldosterone
Excretion of toxic waste products (urea, creatinine…)

Acute renal failure = rapid deterioration of kidney function with rising urea (>10mg/dl) and rising
creatinine (>1mg/dl) + deterioration in GFR (because there are many reasons that will elevate the urea
and creatinine but kidneys are normal  Pseudo acute renal failure

- Increased Urea (with normal creatinine and normal GFR): dehydration OR Upper GI bleeding.
Upper GI bleeding resembles a high protein diet  increased Urea production.
- Increased Creatinine (with normal urea and GFR): due to muscle damage: trauma,
rhabdomyolysis,

Humans are born with a normal FGR ranging from 75 – 120 until age 40 years old, then starts to
deteriorate at rate of 1 unit/year.

Renal failure can be classified into acute & chronic: How to differentiate Acute from Chronic?

Criteria Acute Chronic

Severe vomiting (urea is a potent emetic Absence of vomiting (gradual increase
agent; if it rose rapidly within one day  of urea over long time)
Signs & Symptoms severe vomiting)
- No neuropathy - Neuropathy (urea causes uremic
neuropathy when elevated chronically)
- No anemia - Anemia, low Hb (chronic lack of
erythropoietin)
Lab investigations
- No hypocalcemia - Hypocalcemia (no activation of vit D 
Less Calcium)
Ultrasound Normal sized kidney Small, shrunk kidneys

Acute Renal Failure can be divided according to urine output into anuric, oliguric, and non-oliguric:
Anuric: less 50 ml urine/day
oliguric: less than 300-400 ml urine/day
non-oliguric: more than 400 ml urine/day
Rahaf Wardeh Internal Medicine 2016 - 2017

Renal failure according to causes:

Hemorrhage, dehydration, burns, vomiting, losing fluid,

Hypovolemia
diarrhea …
Heart failure Acute MI, cardiomyopathy, …
Pre Renal
Fluids are in extravascular compartment: ascites,
3rd spacing of fluids
nephrotic syndrome, sepsis..
Renal perfusion shutdown Iatrogenic usually: ACE inh., NSAIDS, ..
Renal artery stenosis/thrombosis
Vessels
Renal vein thrombosis
Acute glomerulonephritis (only those more likely to lead
to renal failure: crescentic GN, GN with rheumatologic
glomerulus
diseases, GN of SLE, Good pasture GN, Churg-Strauss
Syndrome, ANCA positive diseases… )
Renal Cast nephropathy (RBCs, WBCs, tumor lysis syndrome),
tubules crystals, myoglobin, light chain protein (multiple
myeloma), Aminoglycosides!, NSAIDs,
Interstitial nephritis
- medications: penicillin, Sulfonylureas, NSAIDs
Interstitium
- infection: HIV,
- Chinese tea nephropathy
Intraluminal: stone
Intramural: stricture, fibrosis (dt TB for ex)
Ureter obstruction
Post Renal Extramural: tumor, retroperitoneal hematoma or fibrosis,
mass, surgical injury …
Bladder Obstruction Stone, Hematoma/clot from RTA, tumor, BPH…

Clinical Presentation of patients

You should suspect and detect the acute renal failure from the predisposing factors before it actually
happens. You’re very late if you recognize the patient’s status after the failure happened.
Ex. Patient with gastroenteritis with vomiting and loose motion. Patient with 50% burns. Patient with
renal colic. In all these cases and in similar situations, always check hydration status and supplement
fluids if needed to prevent the acute renal failure. So for example, if renal colic patient, you do not
know if there’s obstruction or not. So besides the antispasmodics and analgesics, make sure that the
patient passed urine to know they’re not in failure.

The kidney is very loyal; even when the injury starts stressing the kidney (hypovolemia, obstruction,…)
the kidney will still function properly (pre renal uremia) while sending SOS messages to us (doctors) to
notice the stress and relieve it before the actual necrosis and failure happen.

How to differentiate between pre renal uremia and acute renal necrosis?
Clinically: challenge the kidney with fluids + diuretics. If there’s still urine output, keep going! the kidney
is still functioning and it’s the pre-renal phase. If not, stop fluids before you overwhelm the patient and
cause fluid overload (acute pulmonary edema).
Rahaf Wardeh Internal Medicine 2016 - 2017

Lab workup: a big table you’ll find in books. The concept is that in pre-renal, the kidney is still functional
to some extent, whereas the function is lost in acute renal necrosis. So if this substance stated in the
table is useful to the body, you expect its concentrations to be more in the serum and less in the urine if
the kidney is still functioning, and vice versa. Same concept applies if substance is harmful to the body.
For ex. Water – useful to body. So if urine concentration (osmolarity) is good, means the kidney is still
functional (pre-renal), whereas it is renal failure if urine is diluted (kidney throwing out water). Another
ex. Urea: the normal ratio of urea in urine to blood is 7:1. If it were less than that (4:1 or 3:1) then this is
renal failure. Same goes for creatinine. Another ex. Fractional excretion of sodium (FNa) = what fraction
of the sodium is the kidney capable of retaining. It should be 990/1000 (99%); in other words, no more
than 10/1000 (1%)should be lost in a well-functional kidney. If FNa is 20-30 (2-3%) renal failure.

Management of acute renal failure

Supportive + remove the cause. But you have 6 cases that require urgent dialysis:

- Patient managed but NO URINE OUTPUT.  Acute pulmonary edema.

- Comatose patient with very high urea (uremic encephalopathy).

- Patient with pericardial/pleural rub  serositis.

- Very very high urea in lab workup. Ex. 70.

- Severe acidosis non responsive to treatment. Ex. pH 6.8 not responsive to bicarbonate.

- Hyperkalemia. K+ > 6.5 or <6.5 but with ECG changes (in order if not treated):
Tall tented T wave in all leads. (Pointed, not blunted)
Flattening or depression of P wave.
Prolongation of PR interval.
Widening of QRS complex.
Ventricular arrhythmia and arrest.

Treatment: insulin & dextrose + calcium gluconate to buy time and protect the heart as you
correct the K+ (it doesn’t lower the K+ ).

Remember it’s more important to be a safe doctor, not a smart one!