Medicine — Nephrology, NMC MBBS licence examination syllabus (Nepal Medical Council).
Acute kidney injury and chronic kidney disease
Most acute kidney injury is caused by something the patient was given.
Renal failure sounds like a disease of the kidney. Far more often it is a disease of everything around the kidney — a blood pressure that fell, an infection that took hold, a drug that was prescribed, an outflow that quietly blocked. The kidney is frequently the organ that reports the problem rather than the organ with the problem.
That is why the first question in acute kidney injury is never "what is wrong with the kidney?" but "where is the problem — before it, in it, or after it?" Answer that and the management follows, because the three answers require completely different actions.
🩺 Where this lives: A frail patient on an ACE inhibitor and a diuretic gets a diarrhoeal illness, and someone adds ibuprofen for the accompanying aches. That combination — often called the "triple whammy" — removes the three mechanisms the kidney uses to defend its perfusion when volume falls: the ACE inhibitor blocks efferent arteriolar constriction, the NSAID blocks afferent dilation, and the diuretic empties the tank. None of the drugs is wrong on its own. Together, during dehydration, they take a modest illness and turn it into dialysis.
Where is the problem?
Note the arithmetic buried in that figure. Pre-renal causes are the commonest and are reversible if caught early; post-renal causes are less common but the most completely reversible of all, often by nothing more than a catheter. So the two things that most change a patient's outcome — restore perfusion, exclude obstruction — are both cheap, quick, and done before any sophisticated diagnosis is reached.
HOW THE KIDNEY DEFENDS ITSELF — and how drugs disarm it
When renal perfusion pressure falls, the glomerulus
maintains filtration by:
DILATING the AFFERENT arteriole
→ mediated by PROSTAGLANDINS
→ blocked by NSAIDs
CONSTRICTING the EFFERENT arteriole
→ mediated by ANGIOTENSIN II
→ blocked by ACE inhibitors and ARBs
Both mechanisms hold the pressure gradient ACROSS the
glomerulus. Remove either during hypovolaemia and
filtration collapses.
This single diagram explains why NSAIDs, ACE inhibitors
and ARBs appear in nearly every AKI question — and why
they are held during acute illness rather than stopped
forever.
Recognising and staging
AKI IS DEFINED BY A CHANGE, NOT A THRESHOLD
A RISE in serum creatinine over hours to days
or
A FALL in urine output below roughly 0.5 mL/kg/hour,
sustained
Staging is by the magnitude of the creatinine rise and
the duration of oliguria, in increasing severity.
WHY CREATININE IS A LAGGING, IMPERFECT MARKER
It rises only AFTER filtration has already fallen
→ a "normal" creatinine early does not exclude AKI
It depends on MUSCLE MASS
→ an elderly, cachectic or malnourished patient can
have substantially reduced function with a creatinine
that still reads within the normal range
So a creatinine of 95 may be normal in a young athlete
and represent significant impairment in a frail 80-year-old.
Read the TREND, and read it against the patient.
Pre-renal or established damage?
💡 Exam angle: muddy brown granular casts are the classic urinary finding in acute tubular necrosis and appear regularly in questions. A bland urinalysis with concentrated, sodium-poor urine points to pre-renal azotaemia. Red cell casts point somewhere else entirely — to glomerulonephritis — and change the whole differential toward an intrinsic renal disease requiring specialist input.
Treating what kills first
The hyperkalaemia sequence is worth committing to memory precisely, because each step does a different job and they are frequently confused. Calcium stabilises the myocardium and does not lower potassium at all.Insulin with glucose shifts potassium into cells — the level falls, but the potassium is still in the body and will come back out. Only dialysis or a binder removes it. A question offering "insulin and dextrose" as definitive management of severe hyperkalaemia in an anuric patient is testing exactly that distinction.
GENERAL MANAGEMENT OF AKI
ASSESS VOLUME STATUS and correct it — fluids if
depleted, and equally, do NOT
flood an overloaded oliguric
patient
STOP NEPHROTOXINS NSAIDs, ACE inhibitors, ARBs,
aminoglycosides, contrast where
avoidable
REVIEW EVERY DRUG many need dose reduction in
renal impairment; some (such as
metformin) are held
EXCLUDE OBSTRUCTION ultrasound, bladder scan,
catheter if indicated
TREAT THE CAUSE sepsis is the commonest driver
MONITOR potassium, acid–base, fluid
balance, urine output
ESCALATE renal referral for suspected
intrinsic disease, or dialysis
by the AEIOU criteria
Diuretics do NOT treat AKI. They may be used for fluid
overload, but they do not improve renal recovery, and
using them to "make urine" in a hypovolaemic patient
makes the injury worse.
Chronic kidney disease
CKD is abnormal kidney structure or function present for more than three months. The distinction from AKI matters because the management is entirely different — and because the two are frequently confused at first presentation.
🔍 Telling chronic from acute
Previous resultsThe most useful test of all is an old creatinine. A blood test from two years ago settles the question in seconds.
Small kidneys on ultrasoundChronic scarring shrinks kidneys. Normal or large kidneys with renal failure suggest an acute process — or specific chronic causes such as diabetes, amyloid or polycystic disease.
AnaemiaNormocytic anaemia from erythropoietin deficiency takes time to develop, so it suggests chronicity.
Renal bone diseaseRaised phosphate with raised parathyroid hormone develops over months to years.
SymptomsCKD is often asymptomatic until advanced; acute uraemia produces nausea, confusion and pericarditis more abruptly.
CLASSIFYING AND TREATING CKD
STAGED BY TWO AXES
eGFR — the G stages, from near-normal to end-stage
ALBUMINURIA — the A stages, by albumin:creatinine ratio
Both matter independently. A patient with a preserved eGFR
but heavy albuminuria is at substantial risk, which is why
proteinuria is measured rather than assumed.
COMMONEST CAUSES
Diabetes and hypertension dominate worldwide.
Then glomerulonephritis, polycystic kidney disease,
obstructive uropathy, and chronic interstitial disease.
WHAT SLOWS PROGRESSION
Blood pressure control
ACE inhibitor or ARB where there is proteinuria —
accepting a small, expected creatinine rise on
starting, which reflects the intended haemodynamic
effect rather than harm
SGLT2 inhibitors — renal protection beyond glucose
lowering, connecting back to the diabetes chapter
Avoid nephrotoxins; treat the underlying cause
MANAGING THE CONSEQUENCES
Anaemia — iron first, then an erythropoiesis-stimulating
agent
Mineral and bone disease — phosphate binders, vitamin D
Acidosis — oral bicarbonate
Fluid and potassium — restriction and diuretics
Plan for dialysis or transplantation well in advance
💡 Exam angle: a small rise in creatinine after starting an ACE inhibitor is expected and acceptable — it reflects the intended reduction in intraglomerular pressure, which is the mechanism by which the drug protects the kidney long term. Stopping the drug for that rise removes the protection. A large or progressive rise is different and warrants investigation, including for renal artery stenosis. Questions test whether you can tell the expected effect from the warning sign.
Clinical reasoning: four presentations
🔍 Case 1 — the drug combination
PresentationAn 80-year-old on ramipril and furosemide has three days of vomiting and diarrhoea, and has been taking ibuprofen for aches. Creatinine 310, up from a baseline of 95. Dry mucous membranes, postural drop.
Key cluesVolume depletion plus three drugs that each disable a renal defence mechanism.
ReasoningPre-renal AKI. The diuretic depletes volume, the ACE inhibitor blocks efferent constriction, the NSAID blocks afferent dilation — so the glomerulus cannot maintain filtration when perfusion falls.
AnswerIntravenous fluid resuscitation, hold all three drugs, exclude obstruction, monitor potassium. Caught early this reverses in days; left alone it becomes ATN and takes weeks.
🔍 Case 2 — the shifting answer
PresentationAn anuric patient with AKI has potassium 7.4 and peaked T waves. Calcium gluconate and insulin–dextrose are given; potassium falls to 5.6. A colleague considers the problem solved.
TrapA falling number reading as a resolved problem.
ReasoningInsulin shifts potassium into cells; it does not remove any from the body. In an anuric patient there is no route of excretion, so the potassium will re-equilibrate and rise again within hours.
AnswerArrange definitive removal — urgent dialysis, or a potassium binder if appropriate — and continue monitoring. Stabilise, shift, then remove: all three steps.
🔍 Case 3 — the reversible cause
PresentationA 76-year-old man with a long history of poor urinary stream presents with creatinine 480 and minimal urine output. Abdomen distended and dull suprapubically.
Key clueObstructive symptoms and a palpable bladder — the problem is after the kidney.
ReasoningPost-renal AKI from chronic retention, most likely prostatic. Every hour of continued obstruction costs nephrons, and the fix is immediate.
AnswerBladder scan and urethral catheterisation, then ultrasound for hydronephrosis. Anticipate post-obstructive diuresis — a large diuresis after relief that needs fluid and electrolyte replacement, and can itself cause harm if ignored.
🔍 Case 4 — expected or alarming?
PresentationA patient with diabetic CKD and proteinuria starts an ACE inhibitor. Creatinine rises from 140 to 158 at two weeks. Potassium 4.9, blood pressure improved.
The distractorAny rise in creatinine after a drug looks like drug-induced harm.
ReasoningACE inhibitors dilate the efferent arteriole, lowering intraglomerular pressure. That reduces hyperfiltration — which is precisely the protective mechanism — and produces a small, expected creatinine rise. This one is modest and stable.
AnswerContinue the drug and recheck. A small rise is acceptable and expected; a large or progressive rise, or hyperkalaemia, warrants review and consideration of renal artery stenosis. Stopping it here would discard the long-term renal protection.
Commonly confused
Confusion
The distinction
Why it matters
Pre-renal vs ATN
Pre-renal kidneys concentrate urine and retain sodium
Pre-renal reverses in hours with fluid; ATN takes weeks.
Shifting vs removing potassium
Insulin shifts; only dialysis or a binder removes
Potassium rebounds in an anuric patient.
Calcium vs potassium-lowering
Calcium protects the heart without lowering K⁺
Giving calcium alone leaves the potassium untreated.
AKI vs CKD
Old results, kidney size, anaemia, bone disease
Entirely different management and urgency.
Expected vs alarming creatinine rise on ACE-I
A small stable rise is the intended effect
Stopping the drug discards renal protection.
Normal creatinine vs normal function
Creatinine depends on muscle mass and lags
Frail patients hide substantial impairment.
Muddy brown vs red cell casts
ATN versus glomerulonephritis
They point to different diseases and different specialists.
Rapid revision
MUST-KNOW FACTS
1. First question in AKI: pre-renal, intrinsic, or post-renal?
2. Pre-renal is the commonest; post-renal is the most completely reversible.
3. ALWAYS exclude obstruction early — ultrasound and bladder scan.
4. Pre-renal and ATN are a continuum; prompt treatment prevents the second.
5. NSAIDs block afferent dilation (prostaglandins).
6. ACE inhibitors and ARBs block efferent constriction (angiotensin II).
7. NSAID + ACE-I + diuretic during dehydration is a classic AKI trigger.
8. AKI is defined by a CHANGE in creatinine or urine output, not a threshold.
9. Creatinine LAGS and depends on muscle mass — read the trend.
10. Pre-renal urine: concentrated, low sodium, bland sediment, responds to fluid.
11. ATN urine: dilute, high sodium, MUDDY BROWN casts, no fluid response.
12. RED CELL casts suggest glomerulonephritis — a different disease entirely.
13. Hyperkalaemia ECG: peaked T → wide QRS → sine wave → arrest.
14. Calcium STABILISES the myocardium; it does not lower potassium.
15. Insulin + glucose SHIFTS potassium into cells; it does not remove it.
16. Only DIALYSIS or a binder removes potassium from the body.
17. Dialysis indications — AEIOU: Acidosis, Electrolytes, Intoxication,
Overload, Uraemia.
18. Diuretics do NOT treat AKI or improve recovery.
19. CKD = abnormal structure or function for more than 3 months.
20. Old blood results are the most useful test for distinguishing AKI from CKD.
21. Small kidneys on ultrasound suggest chronicity.
22. CKD anaemia is NORMOCYTIC — erythropoietin deficiency; correct iron first.
23. CKD bone disease: ↑phosphate, ↓active vitamin D, ↓calcium, ↑↑PTH.
24. CKD is staged by BOTH eGFR and albuminuria.
25. A small creatinine rise after starting an ACE inhibitor is expected.
26. Most patients with CKD die of cardiovascular disease.
27. Anticipate post-obstructive diuresis after relieving obstruction.
💡 Exam angle: the reliable threads are (a) locating the problem before, in or after the kidney, (b) the drug triad that disarms renal autoregulation, (c) stabilise–shift–remove in hyperkalaemia, (d) an expected versus an alarming creatinine rise on an ACE inhibitor, and (e) muddy brown versus red cell casts. Once again, several of them turn on a number moving in a way that looks bad and is not, or looks fixed and is not.
Syllabus points
Pre-renal, intrinsic and post-renal: locating the problem
How the glomerulus defends filtration, and how drugs disarm it
Defining and staging AKI
Why creatinine lags and depends on muscle mass
Pre-renal azotaemia versus acute tubular necrosis
Urinary casts and what they indicate
Hyperkalaemia: stabilise, shift, remove
Indications for dialysis
General management and drugs to hold
Distinguishing chronic kidney disease from AKI
CKD: excretory, endocrine and bone consequences
Slowing progression and the ACE inhibitor creatinine rise
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