Medwiki

L12 Renal Acute kidney injury (AKI)

Acute Kidney Injury — Walker

This lecture builds a physiology-first understanding of acute kidney injury (AKI). It defines AKI, classifies it by cause, and grounds the whole topic in the regulation of glomerular perfusion (autoregulation, tubuloglomerular feedback, myogenic control, and the RAAS). It then traces how disturbed perfusion progresses to acute tubular necrosis, and works through three clinical cases (volume depletion via an ileostomy, obstruction from a prostatic abscess, and cardiorenal syndrome) to show how the pathophysiology drives assessment and management. It closes with investigation principles (distinguishing low-perfusion AKI from intrinsic renal and obstructive causes), management, dialysis indications, and the long-term link between AKI and chronic kidney disease (CKD).

Definition and Identification of AKI

  • Understand the definition of AKI: an abrupt reduction in kidney function within 48 hours.
  • Know the diagnostic criteria (“rule of 3”):
    • absolute rise in serum creatinine >27 µmol/L (from normal baseline), OR
    • a >50% rise in serum creatinine over 7 days, OR
    • oliguria <0.5 ml/kg/hr (<35 ml/hr) for >6 hours
  • Understand that decreased urine output is an important component of AKI, not just a rise in creatinine.

Classification of AKI by Cause

  • Understand the three core causal categories the lecture returns to repeatedly:
    • Low perfusion (haemodynamic) AKI
    • Inflammation or nephrotoxins (intrinsic renal)
    • Obstruction (post-renal)
  • Understand: if low perfusion is prolonged, it progresses to acute tubular necrosis (ATN). This is the central narrative thread of the lecture.
  • Know the detailed cause framework (phenotype = cause = “initiation”):
    • Low Perfusion AKI — the “3 Vs”:
      • Vascular — dilation, local (hepatorenal syndrome, sepsis) or systemic (shock); constriction (eclampsia, hypertension, rhabdomyolysis, contrast); raised abdominal pressure reducing arterial and venous flow
      • Ventricular — left (LVF); right (RVF, CCF)
      • Volume — decreased (dehydration); increased but ineffective (congestive states, hypoalbuminaemia)
    • Inflammatory/Immune — sepsis, nephritis (glomerulonephritis, interstitial), vasculitis (systemic or kidney-specific)
    • Obstructive — multiple possible locations
    • Nephrotoxic/Envenomation — direct (toxin-specific = acute tubular injury, ATI); indirect (acute interstitial nephritis, AIN)

Glomerular Filtration and Autoregulation

  • Understand the pressures governing glomerular filtration: glomerular capillary pressure (~45 mmHg) opposed by intracapsular pressure (~10 mmHg) and colloid osmotic pressure (~25 mmHg), giving a net ultrafiltration pressure of ~10 mmHg.
  • Understand that minor changes in perfusion pressure can reduce GFR, which is why perfusion is tightly regulated.
  • Understand autoregulation: intraglomerular pressure (and therefore GFR) is held relatively constant despite changes in systemic arterial pressure.
  • Understand: in chronic hypertension (with or without chronic renal disease) the autoregulation curve is shifted to the right — the kidney depends on a higher MAP to maintain normal intraglomerular pressure.
  • Understand the relationship of renal blood flow (RBF) and GFR to mean arterial pressure (MAP): both are maintained over a plateau, but fall once pressure drops below the autoregulatory range.

Tubuloglomerular Feedback (TGF) and the Juxtaglomerular Apparatus

  • Understand the juxtaglomerular apparatus (JGA) as a vascular system that regulates peripheral vascular resistance, blood pressure and glomerular filtration, while responding to tubular NaCl load and reabsorption rate.
  • Understand the evolutionary logic stated in the lecture: kidney homeostasis = blood pressure homeostasis = salt and water homeostasis, mediated by TGF.
  • Understand that the macula densa senses luminal NaCl via the NKCC2 transporter, and that the JG cells act as a pressure-sensing area analogous to aortic baroreceptors.
  • Understand the LOW NaCl response (tendency for BP to fall):
    • low Na⁺ sensed at macula densa → renin release from JG cells
    • afferent arteriolar vasodilation
    • renin → ↑ angiotensin II → efferent arteriolar vasoconstriction
    • net effect: maintained/raised glomerular capillary pressure → preserved GFR
    • ↑ proximal tubule NaCl reabsorption and raised systemic BP (restoration toward normal)
  • Understand the HIGH NaCl response (tendency for BP to rise) — the “balancing act”:
    • high Na⁺ sensed at macula densa → renin suppressed
    • afferent arteriolar vasoconstriction (mediated via adenosine) to reduce pressure transmission to the glomerulus
    • efferent arteriolar vasodilation
    • net effect: small reduction in GFR, ↓ proximal NaCl reabsorption (due to lower Ang II), systemic BP returned to normal
  • Understand: both responses restore GFR — this is autoregulation in action.

Myogenic Control and the Balance of Vasoactive Mediators

  • Understand myogenic constriction: vasoconstriction to maintain perfusion pressure; pre-glomerular vessels are an important protective mechanism preventing transmission of systemic pressures to the glomeruli.
  • Understand: normal control of renal perfusion = TGF plus myogenic factors, working as a continuous balance of vasoconstricting and vasodilating hormones released tonically at low doses to maintain vascular tone.
  • Know the key mediators:
    • Vasoconstrictors — angiotensin II, noradrenaline/adrenaline (catecholamines, SNS), AVP, endothelin
    • Vasodilators — prostaglandins, nitric oxide
  • Understand: final GFR is a balance of these actions, not independent effects. Specifically:
    • GFR ↑ with afferent dilation (prostaglandins, kinins, low-dose dopamine, ANP, NO) and/or efferent constriction
    • GFR ↓ with afferent constriction (high-dose Ang II, noradrenaline/SNS, endothelin, adenosine, vasopressin, PG blockade) and/or efferent dilation (e.g. Ang II blockade)

The Stress (Hypoperfusion) Response — Pathophysiology

  • Understand that a fall in afferent arteriolar pressure triggers renin release in under 1 second.
  • Understand that angiotensin II directly constricts both pre- and post-glomerular vessels, and that pressure-dependent changes in the renin–angiotensin system are a major cause of the hypotensive resetting of RBF autoregulation.
  • Understand: at a pathophysiological level, marked Ang II activity produces a large reduction in renal perfusion — decreased GFR and decreased vasa recta blood flow.
  • Understand the Ang II / SNS effects on the tubule:
    • ↑ NaCl reabsorption in the proximal tubule (and modulation of distal Na⁺/H⁺ exchange) — an attempt to expand blood volume
    • low distal NaCl load further drives renin–angiotensin release via TGF
    • ↑ metabolism and ↓ tissue oxygen tension — relevant because Na⁺/ATPase has an obligatory oxygen requirement

Altered Perfusion as a Cause of AKI

  • Understand: in the normal kidney, perfusion is tightly regulated to keep glomerular pressure constant despite swings in systemic BP — but any cardiovascular instability compromises autoregulation.
  • Know the factors that limit autoregulatory protection and predispose to hypoperfusion AKI: older age, chronic kidney disease, cardiovascular and peripheral vascular disease (hypertensive or diabetic vasculopathy), ischaemic heart disease, atherosclerosis, hypertension, sepsis.
  • Understand the critical threshold: maximal afferent arteriolar vasodilation occurs at a MAP of ~80 mmHg; below this, afferent arterioles cannot dilate further and renal perfusion begins to fall.
  • Understand the clinical tension: clinically significant hypotension is often defined as MAP <65 mmHg (anaesthetics/ICU), but renal perfusion may already be compromised above that — at MAP 80 mmHg.

The Problem with Mean Arterial Pressure (MAP)

  • Know the formula: MAP = ⅓ SBP + ⅔ DBP.
  • Understand the worked example and why an absolute MAP can mislead:
    • A 70-year-old with BP 160/90 → MAP 113 mmHg (chronically hypertensive, right-shifted autoregulation)
    • When acutely unwell at BP 110/70 → MAP 83 mmHg
    • Although 83 mmHg looks “acceptable,” for a patient whose autoregulation is set higher, this represents a fall that may compromise renal perfusion — i.e. “normotensive renal failure.”
  • Apply: judge perfusion relative to the patient’s usual pressure, not against a single population threshold.

NSAIDs, ACEI/ARB, Diuretics — the “Triple Whammy”

  • Understand how NSAIDs worsen AKI in a vasodilatory insult: inhibition of prostaglandin formation (at the vasculature and macula densa) removes the afferent vasodilation that defends RBF and GFR → medullary ischaemia → ATN.
  • Understand the “Triple Whammy” myth: ACEI/ARB plus diuretics plus NSAIDs are NOT directly nephrotoxic.
    • They reduce the kidney’s ability to compensate for acute drops in perfusion.
    • They do not cause direct tubular injury; they potentiate hypoperfusion of the vasa recta, which can then lead to ischaemic injury (ATN).
    • It is safe to restart ARB/ACEI as the AKI recovers.

Progression to Acute Tubular Necrosis (ATN)

  • Understand: prolonged hypoperfusion (or nephrotoxic insult) → acute tubular necrosis, the link between a functional/haemodynamic problem and structural injury.
  • Understand the histological hallmark: a normal glomerulus alongside necrotic tubular epithelial cells (contrast with normal tubular epithelium).
  • Understand the target areas for early ischaemic injury and why they are vulnerable:
    • Tubules — late proximal tubule and medullary thick ascending limb (MTAL): rich in mitochondria and highly active in transport, so high O₂ demand
    • Vascular endothelium
    • Injured cells undergo necrosis, apoptosis, or sublethal injury.
  • Understand the corticomedullary oxygen gradient and why the medulla is at risk:
    • cortex oxygenated at pO₂ ~50 mmHg; medulla hypoxic at pO₂ ~10–20 mmHg
    • medullary hypoxia arises from countercurrent exchange of O₂ in the vasa recta
    • basolateral Na⁺/ATPase in tubular epithelial cells has an obligatory O₂ requirement, so transport-heavy segments are first to suffer when O₂ falls

Self-Perpetuating Injury and Tubular Obstruction

  • Understand the vicious cycle of established AKI: ischaemia → endothelial cell activation/dysfunction/injury/detachment → impaired vasodilation, coagulopathy, leukocyte adhesion → capillary obstruction and continued ischaemia → inflammation → extension of ARF (which feeds back into more ischaemia).
  • Understand the continuum of tubular injury and why early recognition matters: at-risk kidney → incipient AKI → clinical AKI → dialysis-requiring AKI. Early recognition allows rapid renal recovery; late recognition allows progression to more severe AKI.
  • Understand the mechanism of ischaemic ATN at cell level: O₂/ATP depletion and metabolic changes → loss of microvilli (brush border), cytoskeletal disruption, mislocation of integrins and Na⁺/K⁺-ATPase, denuded tubular walls, backleak of fluid, apoptosis/necrosis, and an inflammatory response (cytokines, reactive oxygen species, leukocyte infiltration).
  • Understand: tubular obstruction by casts (including polymerised Tamm–Horsfall protein) raises intraluminal pressure and leads to oliguria and decreased renal function.

Case 1 — Volume Depletion via Ileostomy

  • Apply the clinical setup: 79-year-old man, total colectomy + end ileostomy for colonic adenocarcinoma, background hypertension (pre-op 156/88), discharged at 7 days with only generic safety-net advice.
  • Understand the physiological pitfall: an ileostomy loses the colon’s water-reabsorbing function — remember the difference between ileum and colon in handling fluid, so stomal losses can be high.
  • Apply the presentation on readmission (14 days later, after collapses with presyncope): tachypnoeic, tachycardic, afebrile, very dehydrated, BP 76/40 sitting, JVP 0 cm lying flat, 4 kg weight loss → admitted to ICU.
  • Understand the terminology correction: it is more accurate to say “low intravascular volume” than simply “dehydration.”
  • Know the dangerous biochemistry: K⁺ 9.0, creatinine 1562, eGFR 3, Na⁺ 131, blood gas pH 7.12 — life-threatening hyperkalaemia and metabolic acidosis on a background of AKI.
  • Understand the ECG progression of hyperkalaemia and its lethal endpoint: rising K⁺ produces characteristic ECG changes, and ventricular fibrillation → death is a potential consequence.
  • Know the management used and the rationale for each:
    • IV fluids (NaCl and NaHCO₃) to correct intravascular volume depletion and metabolic acidosis
    • calcium gluconate to stabilise the cardiac membrane/rhythm
    • insulin + dextrose to shift K⁺ intracellularly
  • Understand the outcome and its physiology: rapid resolution of the filtration failure and acidosis, but a delayed fall in creatinine — reflecting prolonged creatinine half-life plus superimposed tubular injury (ATN).
  • Understand why hyperkalaemia developed:
    • metabolic acidosis drives intracellular K⁺ out (a fall in pH of 0.1 raises K⁺ by ~0.3 mmol/L)
    • reduced tissue perfusion → anaerobic metabolism → lactate + H⁺ → acidosis
    • loss of HCO₃⁻ and the kidney’s role in K⁺ elimination/HCO₃⁻ regeneration
    • the lecture’s key point: acidosis from hypoperfusion is the major mechanism; kidney injury is a late component
  • Apply the take-home: this was preventable AKI — secondary to profound volume depletion (hypoperfusion as major aetiology), with the acute component reversed by IV fluids and slow recovery reflecting ATN; stomal output was later reduced from 3 L/day to ~1 L/day with loperamide. Good communication and monitoring would have prevented it.

Case 2 — Obstruction (Prostatic Abscess)

  • Apply the setup: 74-year-old man, poor urine output, prior radiation and surgery for rectal cancer 6 months earlier, euvolaemic, BP 160/80, JVP 3 cm — creatinine 920.
  • Understand: euvolaemia plus poor urine output should move obstruction and intrinsic renal causes up the differential, not just low perfusion.
  • Know the principles of investigation the lecture lays out:
    • identify low-perfusion AKI and distinguish it from intrinsic renal AKI
    • assess intravascular volume (BP, JVP)
    • identify renal toxic and immunologic causes (urine dipstick and microscopy)
    • exclude post-renal obstruction (history of surgery/catheter, percussable bladder, ultrasound)
  • Understand the obstruction mechanism: obstruction raises tubular back-pressure, reducing the net ultrafiltration gradient and causing a progressive fall in GFR.
  • Understand: anuria = obstruction until proven otherwise.
  • Apply the diagnostic findings: ultrasound showed bilateral hydronephrosis, normal-sized kidneys, large-volume bladder; catheterisation drained 1200 ml; CT pelvis showed no recurrence; MR pelvis showed a probable prostatic abscess causing bladder outlet obstruction.
  • Understand the resolution: relief of obstruction (catheter) plus IV fluids → rapid reversal of creatinine, with post-obstructive diuresis (~6 L/day).

The Recovery Phase of AKI

  • Understand that the recovery (polyuric) phase carries serious risk: 25–50% of mortality occurs in this period.
  • Understand the physiology of post-AKI / post-obstructive polyuria (up to 5 L/24 hr):
    • loss of the medullary concentration gradient
    • lack of tubular response to AVP (ADH)
    • osmotic diuresis
  • Apply the management priorities: watch intravascular volume (JVP, BP) and electrolytes — hypokalaemia and hyponatraemia are characteristic. Recovery can take up to 28 days.
  • Understand the cellular recovery sequence after ischaemic AKI: normal epithelium → loss of brush border and polarity → necrosis/apoptosis → sloughing of viable and dead cells with luminal obstruction → dedifferentiation of viable cells → proliferation → redifferentiation and re-establishment of polarity.

Investigation — Distinguishing the Causes

  • Apply assessment of the low-perfusion state (described as “critical”): assess intravascular volume status, perfusion pressure and cardiac output.
    • postural (lying and standing) BP for postural hypotension
    • JVP (emphasised heavily as the key sign of intravascular volume)
    • body weight: in volume depletion, weight loss approximates the fluid deficit
  • Understand the JVP measurement principle: at 45° measure vertical height from the sternal angle (≈ right atrium, ~3 cm below sternal angle); if lying flat, the reference becomes the centre of the chest (mid-axillary line). With low intravascular volume the JVP may not be visible at 45° and only appears below the clavicle when flat — recorded as 0 cm.
  • Know the urine osmolality discriminators:
    • hypovolaemic stress stimulates ADH → concentrated urine = a normal tubular response
    • urine osmolality >500 mosmol/kg strongly suggests low-perfusion AKI
    • loss of concentrating ability is an early, frequent finding in AKI
    • urine osmolality <450 (usually <350) mosmol/kg suggests ATN
  • Know the urinary sodium discriminators:
    • low urine Na⁺ in low-perfusion AKI (RAAS conserving sodium) — but be aware this can be a pathological response, as in CHF
    • high urine Na⁺ (>40 mmol/L) in ATN due to tubular cell injury
    • overlap occurs because of variations in water reabsorption
  • Know the post-renal assessment: sites and causes of obstruction —
    • extrinsic: pelvic malignancy, para-aortic nodes, prostatic hypertrophy, renal calculi (in a single kidney)
    • intrinsic: tumour lysis with uric acid precipitation, excess oxalate (vitamin C)
    • examination: abdomen, PR/PV; investigations: ultrasound, urine microscopy
  • Know the intrinsic renal sources of injury: drugs (aminoglycosides, cisplatin), toxins (ethylene glycol), sepsis, immunologic (glomerulonephritis, vasculitis). Investigations: urinalysis, biochemistry, renal biopsy.
  • Know the lecture’s specific caution: radiological contrast is NOT a cause of AKI (as taught here).

Case 3 — Cardiorenal Syndrome

  • Apply the setup: 65-year-old man with acute decompensated congestive heart failure; creatinine rises from 136 to 198 µmol/L. Ask why this is AKI, using cardiac pathophysiology.
  • Understand the compensatory changes in untreated CHF that maintain arterial BP: cardiac output and RBF/GFR fall, while total body water, total body sodium, extracellular and plasma volume, and right/left atrial pressures all rise — i.e. neurohormonal activation produces renal dysfunction.
  • Understand the dual haemodynamic pathways to cardiorenal syndrome:
    • Arterial underfilling — decreased cardiac output → decreased effective circulating volume → ↓ RBF/RPF → activation of RAAS and SNS → inflammatory pathways
    • Venous congestion — venous hypertension and raised intra-abdominal pressure → decreased arteriovenous perfusion gradient across the kidney → interstitial oedema → RAAS/SNS activation → inflammation
  • Understand the unifying sequence (heart failure and sepsis both trigger it): a threatened/low BP unloads high-pressure baroreceptors (aortic arch, carotid bodies) → ↑ AVP, ↑ sympathetic output, ↑ renin–angiotensin → ↑ aldosterone, ↓ RBF, ↓ GFR → ↑ proximal and distal tubular Na⁺ reabsorption → Na⁺ and water retention → extracellular volume expansion and oedema, with impaired escape from aldosterone and resistance to natriuretic peptides.
  • Understand the venous-side glomerular mechanism: elevated venous pressure reduces the arteriovenous gradient (= reduced renal perfusion pressure), raises Bowman’s hydrostatic pressure and intratubular pressure, and so decreases net filtration pressure and GFR.
  • Know the definition of cardiorenal syndromes: disorders where acute or chronic dysfunction of the heart or kidney induces dysfunction in the other.
    • progressive LVF → ↓ cardiac output → ↓ systemic perfusion → ↓ renal function (note: mitral regurgitation is a consequence, not the cause)
    • progressive RVF → back-pressure → kidney interstitial oedema with peripheral oedema
    • the failing heart activates RAAS, SNS, AVP → vasoconstriction, salt/water retention, intravascular expansion; by Starling’s law → peripheral oedema; raised afterload / left atrial pressure → pulmonary oedema

Management of Cardiorenal Syndrome / CHF

  • Understand the (counter-intuitive) rationale for ACEI or ARB despite low BP in heart failure: they decrease afterload → improve cardiac output → which in turn improves BP and renal perfusion, and also promote natriuresis (Frank–Starling logic).
  • Know the broader CHF management the lecture lists:
    • diuretics — furosemide at increased dose with continuous blockade twice daily (deliberately not morning + lunchtime)
    • SGLT2 inhibitors — empagliflozin
    • switch ACEI/ARB to sacubitril/valsartan (ARNI — angiotensin receptor–neprilysin inhibitor)
    • mineralocorticoid receptor antagonist — spironolactone

General Management Principles of AKI

  • Understand the low-perfusion / “3 Vs” management logic — correct the underlying cause of hypotension:
    • volume depletion → restore intravascular volume
    • systemic vasodilation (sepsis) → restore pressure (vasopressors such as noradrenaline once volume restored / JVP normal but BP still low)
    • poor cardiac output (ventricular) → correct cardiac output
  • Apply key rules:
    • do NOT give IV saline for heart failure
    • do NOT give diuretics simply to create urine output
    • correct electrolyte and acid–base abnormalities
  • Understand that fluid overload and interstitial oedema can themselves maintain AKI: renal oedema raises interstitial and tubular pressure, reduces the ultrafiltration gradient, and raises renal vascular resistance (worsened by raised venous and intra-abdominal pressure).
  • Know post-renal management: relieve obstruction (catheter, percutaneous nephrostomy, ureteric stents, stone/tumour removal) and anticipate post-obstructive diuresis (5–10 L/24 hr) with its risk of volume depletion and electrolyte disturbance.
  • Know intrinsic renal management: remove/treat the source (sepsis, drugs, toxins); acute glomerulonephritis may need immunosuppression in consultation with nephrology.
  • Know general supportive management: maintain volume and cardiac output (fluid input = previous 24 hr output + ~800 ml insensible losses); avoid sepsis (no unnecessary catheters); early adequate nutrition; renal support with haemodialysis or haemofiltration.

Indications for Dialysis

  • Know the indications:
    • electrolytes — severe hyperkalaemia (arrhythmia risk); metabolic acidosis (potentiates hyperkalaemia and cardiac dysfunction, often severe in sepsis)
    • fluid overload — pulmonary oedema
    • catabolic state
  • Apply the governing principle: treat the cause, not the numbers.
  • Know the mortality figures: AKI carries roughly 30% mortality, largely unchanged over recent decades, and worse with more predisposing factors.
  • Know how survival depends on associated organ involvement:
    • AKI alone: 5–8%
    • AKI + 1 other organ: ~25%
    • multi-organ failure (>3): 80–100%
  • Know the longer-term risks: AKI in ICU confers a 3–4 fold higher risk of death in the first 12 months and a 3–5 fold higher risk of CKD.
  • Understand the severity-dependent recovery of nephrons: mild AKI → full recovery (single-nephron GFR normal, raised CVD risk); moderate → partial GFR recovery, some nephrons lost/regenerated, raised CKD/CVD risk; severe → large GFR loss, remnant nephron hypertrophy, greatly raised single-nephron GFR, raised CKD/CVD/possible cancer risk.
  • Understand the concept of kidney lifespan: AKI shifts the GFR-versus-age trajectory downward, and the impact depends on age at injury (young vs old).
  • Know the absolute risks in the year after an AKI hospitalisation (high-income countries): high all-cause mortality (~28%), plus substantial cardiovascular events, hospital readmission, and new CKD (~20%).
  • Understand the proposed mechanisms linking AKI/CKD to cardiovascular disease: reduced GFR, SNS and RAAS activation, coagulation/endothelial dysfunction, inflammation → neurohormonal activation, volume expansion, hypertension, electrolyte/acid–base imbalance → cardiac remodelling, LV hypertrophy, heart failure, coronary atherosclerosis/calcification/ischaemia, arrhythmias.
  • Understand the key cardio-renal interaction domains: haemodynamic (fluid overload, congestion, limited perfusion, end-organ vasoconstriction), neurohormonal (RAAS and SNS activation), and CVD-associated mechanisms (chronic inflammation, malnutrition/cachexia, bone–mineral and acid–base disorders, anaemia).

Take-Home Points

  • Use the “rule of 3” to identify AKI.
  • Kidney hypoperfusion (low perfusion) is the major cause in most cases.
  • Management is fundamentally about correcting the underlying pathophysiology.
  • AKI is associated with an increased risk of CKD (and cardiovascular disease).

Self-Test Checklist

  • Can you state the three diagnostic criteria for AKI from memory?
  • Can you name the three main causal categories and place each of the “3 Vs” under low-perfusion AKI?
  • Can you explain what autoregulation achieves and how chronic hypertension shifts the curve?
  • Can you walk through the low-NaCl and high-NaCl TGF responses, including which arteriole constricts/dilates and the role of adenosine vs renin/Ang II?
  • Can you list the renal vasoconstrictors and vasodilators and predict their effect on GFR via afferent vs efferent action?
  • Can you explain why maximal afferent dilation at ~80 mmHg matters relative to the MAP <65 mmHg hypotension threshold?
  • Can you calculate MAP and explain why a “normal” MAP can still represent renal hypoperfusion in a chronic hypertensive?
  • Can you explain why the “triple whammy” drugs are not directly nephrotoxic but still cause AKI?
  • Can you explain why the medullary thick ascending limb is especially vulnerable to ischaemia?
  • Can you describe the vicious cycle that perpetuates established AKI?
  • Can you explain how tubular obstruction (casts, Tamm–Horsfall protein) produces oliguria?
  • Can you explain why Case 1’s ileostomy patient developed hyperkalaemia, and the role of acidosis vs kidney injury in it?
  • Can you justify each drug given in Case 1 (calcium gluconate, insulin/dextrose, fluids/bicarbonate)?
  • Can you explain why creatinine falls slowly even after the cause is corrected?
  • Can you distinguish low-perfusion AKI from ATN using urine osmolality and urine sodium?
  • Can you explain why “anuria = obstruction until proven otherwise”?
  • Can you describe post-obstructive (recovery-phase) diuresis and its electrolyte risks?
  • Can you measure and interpret the JVP at 45° and lying flat, including the 0 cm finding?
  • Can you explain the two haemodynamic pathways (arterial underfilling and venous congestion) in cardiorenal syndrome?
  • Can you justify using ACEI/ARB in heart failure despite a low blood pressure?
  • Can you match each AKI cause to the correct management (“3 Vs” logic), and state the two “do NOT” rules?
  • Can you list the indications for dialysis and explain “treat the cause, not the numbers”?
  • Can you quote the survival figures by number of organs involved, and the long-term AKI→CKD/CVD risks?

Graph View