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Home >Nephrology > Acute Kidney Injury (AKI)

Acute Kidney Injury (AKI)

Unlike chronic kidney disease, AKI arrives suddenly - sometimes over hours. A person admitted for surgery, a severe infection, or a medication reaction can find their kidneys shutting down before anyone notices. Sudden kidney function loss is a medical emergency, not a complication to be noted and monitored. At Shree Hospitals, our acute kidney injury treatment in Mumbai is structured around speed and cause identification - because the single most important determinant of renal recovery after AKI is how quickly the triggering insult is identified and reversed. Most AKI is reversible. Most AKI that does not recover was not treated fast enough.

(24×7 Emergency Care)

1800-268-4000

(24×7 Emergency Care)

1800-268-4000

Our Approach in Managing Acute Kidney Injury

The first question in AKI is always: what caused this? Pre-renal, intrinsic renal, or post-renal - the cause determines the treatment, and treating the wrong mechanism wastes time the kidneys do not have. Our AKI specialist nephrologist team in Mumbai, India runs a simultaneous diagnostic and resuscitation protocol from the moment AKI is identified.

AKI Diagnosis & Severity Staging

KDIGO AKI criteria: creatinine rise ≥0.3 mg/dL within 48 hours, or ≥1.5× baseline within 7 days, or urine output <0.5 ml/kg/hour for ≥6 hours
Stage 1: creatinine 1.5–1.9× baseline; Stage 2: 2–2.9× baseline; Stage 3: ≥3× baseline, or initiation of RRT
Urine output monitoring - hourly in ICU setting; reduced output is often the earliest AKI signal
Baseline creatinine determination - previous records or back-calculation from eGFR where unavailable

Identifying the Cause - Pre-Renal, Intrinsic, Post-Renal

Pre-renal AKI - volume depletion (dehydration, haemorrhage, sepsis, cardiac failure, hepatorenal syndrome); BUN:creatinine ratio >20, FENa <1%
Intrinsic renal AKI - ATN (most common), GN, interstitial nephritis, contrast nephropathy, rhabdomyolysis
Post-renal AKI - urinary obstruction from stones, prostate enlargement, malignancy; renal ultrasound is the critical first imaging step
Drug review - NSAIDs, aminoglycosides, contrast agents, ACE inhibitors in volume-depleted patients

Immediate Resuscitation & Cause Reversal

Pre-renal AKI: IV fluid resuscitation - crystalloids for dehydration, blood products for haemorrhage, vasopressors for septic shock
Post-renal AKI: urinary catheter insertion or nephrostomy for obstruction - sudden kidney function loss from obstruction recovers rapidly with timely decompression
Contrast nephropathy prevention: hydration before contrast, use iso-osmolar contrast, withhold nephrotoxins
Rhabdomyolysis: aggressive IV hydration targeting urine output >300 ml/hour to flush myoglobin
Interstitial nephritis: identify and withdraw offending drug; steroids where drug-induced AIN is confirmed

Conservative Management in Established AKI

Once the cause is reversed, the kidney needs support while it recovers.

Fluid balance: daily weight, input-output monitoring - avoid both fluid overload and under-resuscitation
Electrolyte management: hyperkalaemia (most dangerous - ECG monitoring, Calcium gluconate, insulin-dextrose, potassium binders), hyperphosphataemia, metabolic acidosis
Medication dose adjustment - virtually all renally-cleared drugs require dose reduction or interval extension
Nutritional support - adequate caloric intake without excessive protein load; 1.0–1.5g/kg/day protein in ICU AKI

Renal Replacement Therapy (RRT) in AKI

RRT in AKI is a bridge - not a destination. Most AKI patients who receive dialysis recover enough kidney function to come off it.

Urgent indications: severe hyperkalaemia, metabolic acidosis (pH <7.2), refractory fluid overload, uraemic encephalopathy or pericarditis
Modality choice: continuous RRT (CRRT) for haemodynamically unstable ICU patients; intermittent haemodialysis for stable patients
RRT timing - initiate when medical management fails; earlier is not always better without urgent indication
Discontinuation trial when urine output recovers - avoid prolonging RRT beyond clinical need

Post-AKI Care & Recovery Monitoring

Renal recovery after AKI is not always complete - and incomplete recovery significantly increases lifetime CKD risk.

Creatinine and eGFR at 3 months post-discharge - defines recovery vs. AKI-to-CKD transition
UACR at 3 months - new proteinuria post-AKI is a CKD risk signal
Avoid nephrotoxins indefinitely post-AKI - these patients have reduced renal reserve
CKD follow-up if eGFR has not returned to pre-AKI baseline at 3 months

Happy Patients & Their Case Stories

Admitted for an elective knee replacement, Suresh received an NSAID post-operatively and became mildly dehydrated. On day 3, his creatinine rose to 3.2 mg/dL from a baseline of 0.9. AKI stage 3 was diagnosed. NSAIDs were stopped, IV fluids were initiated, and all nephrotoxic medications were withheld. He did not require dialysis. His creatinine returned to 1.1 by day 10.

Mr. Bhargav . K

Presented with severe muscle pain and dark urine three days after an intense gym session combined with a creatine supplement. Creatinine was 8.4 mg/dL, CK was 180,000 U/L. Rhabdomyolysis-induced AKI was diagnosed. He was started on aggressive IV hydration in ICU, developed hyperkalaemia requiring CRRT for four days, then recovered spontaneously.

Mr. Sadashiv . N

How to Identify Acute Kidney Injury?

AKI is most often identified on blood tests - either during hospitalisation or at a routine check at the right moment.

Situations where AKI should be actively excluded:

Any serious illness - sepsis, pneumonia, diarrhoeal illness, cardiac event - check creatinine
After starting a new medication - particularly NSAIDs, antibiotics, or contrast procedures
Following surgery - especially cardiac, vascular, or major abdominal procedures
After a crush injury, severe muscle exertion, or significant blood loss
In a patient with pre-existing CKD, diabetes, or heart failure - these populations are at highest risk
Dark or brown-coloured urine following muscle injury or haemolysis
Inability to urinate despite adequate fluid intake - post-renal obstruction must be excluded within hours

The critical point is that sudden kidney function loss does not cause pain. The only way to catch it is to measure it. In hospitalised patients, creatinine and urine output should be monitored daily when any AKI risk factor is present. If you are at home and notice any of the above - reduced urine, swelling, unusual fatigue after an illness - seek acute kidney injury treatment in Mumbai without delay.

Important FAQs - Acute Kidney Injury

Is AKI always reversible?

Most AKI is reversible when the cause is identified and treated promptly. Severity, duration, and baseline kidney health all influence recovery. Approximately 10–15% of AKI patients develop CKD as a consequence.

How quickly does kidney function recover after AKI?

Pre-renal and post-renal AKI typically recover within days of cause reversal. Intrinsic AKI - particularly ATN - may take 2–6 weeks to recover. Some patients require dialysis during the recovery period before function returns.

Does AKI lead to CKD?

Yes - AKI significantly increases lifetime CKD risk, proportional to severity and number of AKI episodes. Post-AKI follow-up at 3 months is essential to detect incomplete recovery early.

Can AKI be prevented in high-risk patients?

Substantially, yes. Avoiding nephrotoxins, maintaining adequate hydration, using contrast agents cautiously, and monitoring creatinine proactively in at-risk patients prevents a large proportion of avoidable AKI.

When is dialysis stopped in AKI?

When urine output recovers sufficiently (typically >500 ml/day) and creatinine stabilises or begins to fall, a trial off dialysis is appropriate. Most AKI dialysis is temporary.

Treatments for AKI at Shree Hospitals

Comprehensive acute renal failure management in Mumbai from emergency resuscitation to post-AKI recovery monitoring.

IV Fluid Resuscitation

Targeted fluid therapy for pre-renal AKI - crystalloids, colloids, or blood products based on the specific cause of volume depletion. Guided by haemodynamic monitoring to avoid over and under-resuscitation.

Urinary Decompression

Emergency catheterisation or nephrostomy insertion for post-renal obstructive AKI - often producing rapid creatinine rise reversal within 24–48 hours of obstruction relief.

Continuous Renal Replacement Therapy (CRRT)

Slow, continuous dialysis for haemodynamically unstable AKI patients in the ICU. Provides fluid and electrolyte management without the BP fluctuations of intermittent haemodialysis.

Intermittent Haemodialysis

For stable AKI patients with urgent indications - hyperkalaemia, acidosis, fluid overload. A bridge to renal recovery after AKI rather than a long-term commitment.