Library Demo · sample lecture, nothing is saved

Welcome back, doc

6 lectures down, doc!

142 Lectures finished once

11 Flashcards solved to date

SBA correct 86

SBA wrong 14

Renal

Glomerulonephritis Processing

Nephrotic syndrome Failed

Cardiology

Upload a lecture

Drop it like it’s hot

PDF only

Uploading Pending

Reading pages Pending

Writing notes I’m waiting to start writing the notes, sorry about the traffic :(

Making flashcards Pending

Writing SBAs Pending

Notes

ELI5

Flashcards

New12 Due47

Flashcards are locked until every section of your notes is finished.

Pending SBAs

Can’t get these to the Genie, the traffic’s super backed up, doc

SBAs

Question n of N

A 60-year-old man is brought to the emergency department due to altered mental status. His wife says that he has a nagging cough that seemed to worsen over the past several months and that he also began experiencing occasional dizziness earlier this week. Over the last couple of days, the patient has become increasingly confused, and today he “does not make any sense at all.” He has no significant past medical history but has smoked a pack of cigarettes daily for the last 40 years. On physical examination, the patient is incoherent but has an otherwise normal neurologic examination. Chest x-ray reveals a mass in the right lung.

Investigations:

Sodium	120 mEq/L
Potassium	4.0 mEq/L
Blood urea nitrogen	12 mg/dL
Creatinine	0.8 mg/dL
Calcium	9.0 mg/dL
Glucose	98 mg/dL
Plasma osmolality	250 mOsm/kg
Urine drug screen	negative

Which of the following additional findings is most likely to be present in this patient?

PERFECTOMONDO

The StudyFix Genie is very proud of you

Right — 0

Wrong — 0

Question	Your answer	Correct answer

Reference ranges

NBME laboratory reference values

Test	Reference range
Serum — electrolytes
Sodium (Na⁺)	136–146 mEq/L
Potassium (K⁺)	3.5–5.0 mEq/L
Chloride (Cl⁻)	95–105 mEq/L
Bicarbonate (HCO₃⁻)	22–28 mEq/L
Urea nitrogen	7–18 mg/dL
Creatinine	0.6–1.2 mg/dL
Glucose	Fasting: 70–100 mg/dL Random, non-fasting: <140 mg/dL
Calcium	8.4–10.2 mg/dL
Magnesium (Mg²⁺)	1.5–2.0 mg/dL
Phosphorus (inorganic)	3.0–4.5 mg/dL
Serum — hepatic
Alanine aminotransferase (ALT)	10–40 U/L
Aspartate aminotransferase (AST)	12–38 U/L
Alkaline phosphatase	25–100 U/L
Bilirubin, total // direct	0.1–1.0 mg/dL // 0.0–0.3 mg/dL
Proteins, total	6.0–7.8 g/dL
Albumin	3.5–5.5 g/dL
Globulin	2.3–3.5 g/dL
Serum — other
Amylase	25–125 U/L
Lipase	13–60 U/L
Creatinine clearance	Male: 97–137 mL/min Female: 88–128 mL/min
Creatine kinase	Male: 25–90 U/L Female: 10–70 U/L
Lactate dehydrogenase	45–200 U/L
Osmolality	275–295 mOsmol/kg H₂O
Troponin I	≤0.04 ng/mL
Uric acid	3.0–8.2 mg/dL
Serum — lipids
Cholesterol, total	Normal: <200 mg/dL High: >240 mg/dL
HDL	40–60 mg/dL
LDL	<160 mg/dL
Triglycerides	Normal: <150 mg/dL Borderline: 151–199 mg/dL
Serum — iron studies
Ferritin	Male: 20–250 ng/mL Female: 10–120 ng/mL
Iron	Male: 65–175 µg/dL Female: 50–170 µg/dL
Total iron-binding capacity	250–400 µg/dL
Transferrin	200–360 mg/dL
Serum — endocrine
Follicle-stimulating hormone	Male: 4–25 mIU/mL Female: premenopause 4–30 mIU/mL midcycle peak 10–90 mIU/mL postmenopause 40–250 mIU/mL
Luteinizing hormone	Male: 6–23 mIU/mL Female: follicular phase 5–30 mIU/mL midcycle 75–150 mIU/mL postmenopause 30–200 mIU/mL
Growth hormone — arginine stimulation	Fasting: <5 ng/mL Provocative stimuli: >7 ng/mL
Prolactin (hPRL)	Male: <17 ng/mL Female: <25 ng/mL
Cortisol	0800 h: 5–23 µg/dL 1600 h: 3–15 µg/dL 2000 h: <50% of 0800 h
TSH	0.4–4.0 µU/mL
Triiodothyronine (T₃) (RIA)	100–200 ng/dL
Triiodothyronine (T₃) resin uptake	25%–35%
Thyroxine (T₄)	5–12 µg/dL
Free T₄	0.9–1.7 ng/dL
Thyroidal iodine (¹²³I) uptake	8%–30% of administered dose/24 h
Intact PTH	10–60 pg/mL
17-Hydroxycorticosteroids	Male: 3.0–10.0 mg/24 h Female: 2.0–8.0 mg/24 h
17-Ketosteroids, total	Male: 8–20 mg/24 h Female: 6–15 mg/24 h
Serum — immunoglobulins
IgA	76–390 mg/dL
IgE	0–380 IU/mL
IgG	650–1500 mg/dL
IgM	50–300 mg/dL
Arterial blood gases (room air)
PO₂	75–105 mm Hg
PCO₂	33–45 mm Hg
pH	7.35–7.45
Cerebrospinal fluid
Cell count	0–5/mm³
Chloride	118–132 mEq/L
Gamma globulin	3%–12% total proteins
Glucose	40–70 mg/dL
Pressure	70–180 mm H₂O
Proteins, total	<40 mg/dL
Hematologic — complete blood count
Hematocrit	Male: 41%–53% Female: 36%–46%
Hemoglobin, blood	Male: 13.5–17.5 g/dL Female: 12.0–16.0 g/dL
Mean corpuscular hemoglobin (MCH)	25–35 pg/cell
Mean corpuscular hemoglobin conc. (MCHC)	31%–36% Hb/cell
Mean corpuscular volume (MCV)	80–100 µm³
Plasma volume	Male: 25–43 mL/kg Female: 28–45 mL/kg
Red cell volume	Male: 20–36 mL/kg Female: 19–31 mL/kg
Leukocyte count (WBC)	4500–11,000/mm³
Neutrophils, segmented	54%–62%
Neutrophils, bands	3%–5%
Lymphocytes	25%–33%
Monocytes	3%–7%
Eosinophils	1%–3%
Basophils	0%–0.75%
Platelet count	150,000–400,000/mm³
Hematologic — coagulation
Partial thromboplastin time (activated) (PTT/aPTT)	25–40 seconds
Prothrombin time (PT)	11–15 seconds
D-dimer	≤250 ng/mL
Hematologic — other
Reticulocyte count	0.5%–1.5%
Erythrocyte count (RBC)	Male: 4.3–5.9 million/mm³ Female: 3.5–5.5 million/mm³
Erythrocyte sedimentation rate (Westergren)	Male: 0–15 mm/h Female: 0–20 mm/h
CD4⁺ T-lymphocyte count	≥500/mm³
Hemoglobin A1c	≤6%
Urine
Calcium	100–300 mg/24 h
Osmolality	50–1200 mOsmol/kg H₂O
Oxalate	8–40 µg/mL
Proteins, total	<150 mg/24 h
Other
Body mass index (BMI)	Adult: 19–25 kg/m²

Electrolyte Disorders (4)

Nephritic Syndromes (6)

Nephrotic Syndromes (4)

End-Stage GN (1)

Cystic (1)

Interstitial & Toxic (6)

Acute Renal Injury (6)

Vascular (4)

Chronic (1)

UTI & Pyelonephritis (4)

Stones & Reflux (2)

Renal Neoplasms (2)

Renal Replacement Therapy (5)

Diagnostic Criteria (2)

AKI Staging (3)

CKD Staging (2)

Histological Classifications (2)

Anatomical / Severity (1)

Urine Chemistry (2)

Nephro

Electrolyte Disorders

4 entries

Hypernatraemia

C/P

Serum Na > 145 mmol/L → water drawn out of cells → brain shrinks
Predominantly neurological symptoms
Acute (<48 h): symptomatic — confusion, headache, N/V, seizures, coma
Chronic (>48 h): usually asymptomatic (brain adapts by osmotic uptake)

Reveal

Inves

Serum Na — confirm >145 mmol/L threshold
Serum + urine osmolality — high serum osm identifies water-loss vs Na-gain
Water-loss vs Na-gain workup — ADH status (CDI vs NDI), aldosterone/cortisol if Conn's/Cushing's suspected

Reveal

Mng

Water-loss predominant — 5% dextrose IV or oral water + treat cause (e.g. vasopressin for CDI)
Na-gain predominant — diuretics (increase Na loss in urine) + 5% dextrose + treat cause

Reveal

Special

Central DI — ↓ADH from posterior pituitary (idiopathic, trauma, neurosurgery, infection, tumour)
Nephrogenic DI — normal ADH but tubules unresponsive (renal disease, sickle cell, lithium)
Conn's — adrenal cortex tumour → ↑Na, ↑BP, ↓K, metabolic alkalosis
Cushing's — cortisol mineralocorticoid effect (adrenal tumour or corticosteroid intake)
Water-loss causes (beyond DI) — insensible loss (sweating, burns, fever, exercise), GI loss (vomiting, diarrhoea), osmotic diuresis (DKA, diuretics)

Reveal

Hyponatraemia

C/P

Serum Na < 136 mmol/L → water drawn into cells → brain swells
Acute (<48 h): confusion, headache, N/V, seizures, coma
Chronic (>48 h): usually asymptomatic (brain excretes intracellular osmoles)
Severe (<120 mmol/L) — symptomatic regardless of acute or chronic

Reveal

Inves

Serum Na — confirm <136 mmol/L
Serum osmolality — ↓ in true (hypo-osmolar) hyponatraemia
Assess volume status first — hypovolaemic / euvolemic / hypervolemic drives the workup
Urine Na + osmolality — helps localise SIADH vs renal loss
TFTs / short synacthen — rule out hypothyroidism, Addison's

Reveal

Mng

Symptomatic → 3% hypertonic saline (regardless of volume)
Asymptomatic hypovolaemic → 0.9% normal saline + treat cause
Asymptomatic euvolemic / hypervolemic → water restriction + diuretics + treat cause

Reveal

Special

Hypovolaemic — diuretics, Addison's (↓aldosterone → renal Na loss + hyperkalaemia + metabolic acidosis), vomiting/diarrhoea
Euvolemic — SIADH (CNS/pulmonary disease, cancers, SSRIs/TCAs), hypothyroidism, psychogenic polydipsia (15–20 L/day)
Hypervolemic — renal failure, heart failure, liver failure, nephrotic syndrome

Reveal

Hypokalaemia

C/P

Muscle — weakness; paralysis if severe
Cardiac — arrhythmias
Renal — nephrogenic DI (K required for ADH effect on tubule)

Reveal

Inves

Serum K — confirm hypokalaemia
ECG — flat T wave, prominent U wave
Serum Mg — often co-depleted; refractory K unless Mg replaced
Aldosterone / renin — for Conn's, secondary hyperaldosteronism screen
ECG — flat T wave, prominent U wave, ST depression, PR prolongation

Reveal

Mng

Oral K supplementation — mild/moderate deficit with normal ECG
IV KCl — severe hypokalaemia, ECG changes, or unable to take orally; via central line if concentrated
Correct Mg — hypomagnesaemia perpetuates renal K wasting
Treat cause — stop offending diuretic, treat Conn's, replace GI losses
Avoid dextrose-containing IV fluids — use isotonic 0.9% saline as diluent; dextrose triggers insulin release → drives K into cells → worsens hypokalaemia

Reveal

Special

Classic ECG signature — flat T + prominent U wave (opposite of hyperkalaemia's peaked T)
Causes — GI loss (vomiting, diarrhoea); transcellular shift into cells (insulin, β-agonists, alkalosis); renal loss (loop/thiazide diuretics, mineralocorticoid excess, tubular defects)
Tubular-defect causes — Bartter (Na-K-2Cl defect, ascending loop of Henle, mimics loop diuretic), Gitelman (Na-Cl defect, DCT, mimics thiazide), liquorice

Reveal

Hyperkalaemia

C/P

Muscle — weakness
Cardiac — abnormal conduction / heart block

Reveal

Inves

Serum K — confirm; rule out haemolysed sample
ECG — peaked T wave
Renal function (urea/Cr) — CKD/AKI is dominant cause
Blood gas — associated metabolic acidosis
Aldosterone/cortisol — screen Addison's if hyponatraemic + hypotensive
Full ECG progression — peaked T → widening QRS → PR prolongation → low-amplitude P wave
ECG — peaked T wave, widening of QRS, PR prolongation, low-amplitude (flattened) P wave

Reveal

Mng

Calcium gluconate IV — first line if ECG changes; membrane stabilisation, doesn't lower K
Insulin + dextrose — shifts K into cells via Na-K pump; dextrose prevents hypoglycaemia
Sodium bicarbonate — alkalosis drives K into cells in exchange with H+
Beta-2 agonist (nebulised salbutamol) — activates Na-K pump
Loop diuretics — increase urinary K excretion
Cation exchange resin — absorbs K from GIT → excreted in stool
Dialysis — last line if refractory; also for AEIOU indications in AKI

Reveal

Special

Classic ECG signature — peaked T wave, then QRS widening (opposite of hypokalaemia's flat T + U)
Extracellular shift causes — cell lysis (rhabdo, tumour lysis), acidosis, insulin deficiency, beta blockers, digoxin
Decreased-excretion causes — drugs (K-sparing diuretics, ACE-i, ARBs → ↓aldosterone), decreased adrenal activity (Addison's), renal failure

Reveal

Acute Renal Injury

6 entries

Acute Tubular Necrosis (ATN)

C/P

Final common pathway for many insults — accounts for 80–90% of intrinsic AKI
Ischaemic ATN — trauma, septicaemia, acute pancreatitis, hypotension/shock
Nephrotoxic ATN — poisons, drugs (aminoglycosides, contrast agents), organic solvents, myoglobin (rhabdo)
Four classical phases — onset (36 h) → oliguric (few days–3 weeks, marked oliguria + uraemia) → diuretic (polyuria >3 L/day) → recovery (weeks); usually partial residual impairment

Reveal

Inves

Urea/creatinine rising over days
Urine — muddy brown granular casts, renal tubular epithelial cell casts
Urine Na > 20, FENa >1%, urine osm <350 — distinguishes from pre-renal
Ultrasound — normal or enlarged kidneys (rule out post-renal)
Renal biopsy if persistent >4 weeks or unclear cause

Reveal

Mng

DO NOT give fluid in established ATN — supportive only
Withhold nephrotoxins; adjust doses of renally cleared drugs
Treat hyperkalaemia, acidosis, fluid overload, sepsis
RRT — for AEIOU indications: refractory Acidosis, Electrolytes (K >6.5), Intoxications, Overload, Uraemic complications
Recovery over 7–21 days; sepsis delays recovery

Reveal

Special

Nephrotoxic ATN — basement membrane and regeneration? Nephrotoxic ATN — spares basement membrane, targets whole PCT → good regeneration
Ischaemic ATN — basement membrane and regeneration? Ischaemic ATN — focal rupture of tubular basement membrane → incomplete regeneration in those areas
What are the gross findings? Gross — enlarged kidney, pale necrotic cortex, congested medulla
Two oliguria mechanisms — (1) tubular damage → renin-angiotensin → afferent VC → ↓GFR; (2) debris blocks lumen → ↑intratubular pressure → fluid leak to interstitium → collapsed tubules
Non-oliguric AKI usually reflects a less severe renal insult (better prognosis); oliguria is the common early finding

Reveal

Rhabdomyolysis

C/P

Skeletal muscle injury releases myoglobin → nephrotoxic ATN ("crush syndrome")
Causes — trauma, compartment syndrome, excessive exertion (marathon runners), status epilepticus
Muscle toxins — statins, malaria/antimalarials, snake/insect venom
Dark brown / tea-coloured urine + oliguria + AKI

Reveal

Inves

Urine dipstick — positive for blood, but no RBCs on microscopy (myoglobin cross-reactivity)
Elevated markers — K↑, PO4↑, CPK↑↑ (creatine phosphokinase)
Serum myoglobin
Renal function — rising BUN/creatinine consistent with ATN
Assess for compartment syndrome — surgical review

Reveal

Mng

Aggressive IV fluid resuscitation — crystalloids to maintain urine output and flush myoglobin
Treat hyperkalaemia — insulin/dextrose, calcium gluconate for ECG changes
Fasciotomy — if compartment syndrome
Haemodialysis if severe AKI or refractory hyperkalaemia
Tubular epithelium regenerates with supportive care

Reveal

Special

Urine dipstick positive for blood but no RBCs on microscopy — pathognomonic for myoglobin/haemoglobin
What is the classic AKI phase sequence? Classic AKI arc — oliguric maintenance phase → recovery phase polyuria (>3 L/day) as tubules recover before concentrating ability

Reveal

Acute Kidney Injury (AKI)

C/P

Abrupt deterioration in renal function over hours–days, usually reversible
Acute symptoms — dyspnoea, N/V, diarrhoea
Common — 1 in 5 hospitalised adults, 1 in 3 hospitalised children; ~5% UK community admissions; sepsis (25%) or septic shock (50%)
3 anatomical categories — pre-renal (hypoperfusion), renal parenchymal, post-renal (obstruction)
Pre-renal causes — hypovolaemia (dehydration, haemorrhage), hypotension without hypovolaemia (cirrhosis, septic shock), low cardiac output (cardiac failure, cardiogenic shock)
Intrinsic (renal parenchymal) — 4 subtypes: ATN (80–90%), glomerular (acute RPGN), acute tubulointerstitial, vascular (vasculitis, accelerated hypertension, cholesterol embolism, HUS)
Post-renal — prostate disease (men) or bilateral ureteric obstruction (stones/tumours); hesitancy + frequency; palpable bladder + suprapubic dullness on exam
Assess volume status — hypovolaemia signs: low BP, rapid pulse, sunken eyes, collapsed neck veins

Reveal

Inves

Serum urea + creatinine + eGFR — stage per RIFLE/AKIN/KDIGO
Blood urea to creatinine ratio > 20:1 (urea:creatinine >40:1) — suggests pre-renal
Urine chemistry — FENa <1%, urine Na <10, urine osm >500 in pre-renal; opposite in intrinsic
Urinalysis — RBC casts (glomerulonephritis), free Hb/myoglobin, pigmenturia
Early biomarkers — KIM-1, NGAL rise within hours
Serum chemistry — U&E, Ca, PO4, albumin, ALP, urate; CBC, coagulation, blood cultures, nephrotoxic drug levels; immune profile if GN suspected
Ultrasound of abdomen + pelvis — mandatory to exclude obstruction; check bladder
Renal biopsy — indicated if unexplained urine abnormalities (proteinuria/haematuria), persistent ATN >4 weeks, unclear aetiology, suspected systemic disease
Acute vs chronic — kidneys normal size on US in AKI vs small in CKD (except diabetes, where CKD kidneys stay normal/large); previous creatinine normal; anaemia, high PTH, hyperphosphataemia and hypocalcaemia less common than in CKD

Reveal

Mng

Fluid balance — daily weights, lying/standing BP, intake/output; withhold nephrotoxins
Pre-renal — fluid challenge of 250 mL crystalloid; Plasmalyte or Ringer's lactate preferred over 0.9% saline (avoid hyperchloraemic acidosis)
Post-renal — urethral catheter + upper tract imaging; nephrostomy for upper tract obstruction
Intrinsic ATN — DO NOT give fluid once established; supportive
Treat hyperkalaemia, acidosis, pulmonary oedema, sepsis
Adjust drug doses daily; particular care with anticoagulants; salt + K restriction
RRT indications (all 5) — symptomatic uraemia (encephalopathy/pericarditis/tamponade), refractory hyperkalaemia, refractory pulmonary oedema, severe acidosis, drug removal (gentamicin, lithium, severe aspirin overdose)

Reveal

Special

Uncomplicated AKI mortality <5–10%; ITU + multi-organ failure 50–70%; sepsis-associated AKI much worse prognosis
Autoregulation defence — prostaglandins on afferent arteriole (blocked by NSAIDs); angiotensin II on efferent arteriole (blocked by ACE-i)

Reveal

Acute Tubular Necrosis (ATN)

C/P

Final common pathway for many insults — accounts for 80–90% of intrinsic AKI
Ischaemic ATN — trauma, septicaemia, acute pancreatitis, hypotension/shock
Nephrotoxic ATN — poisons, drugs (aminoglycosides, contrast agents), organic solvents, myoglobin (rhabdo)
Four classical phases — onset (36 h) → oliguric (few days–3 weeks, marked oliguria + uraemia) → diuretic (polyuria >3 L/day) → recovery (weeks); usually partial residual impairment

Reveal

Inves

Urea/creatinine rising over days
Urine — muddy brown granular casts, renal tubular epithelial cell casts
Urine Na > 20, FENa >1%, urine osm <350 — distinguishes from pre-renal
Ultrasound — normal or enlarged kidneys (rule out post-renal)
Renal biopsy if persistent >4 weeks or unclear cause

Reveal

Mng

DO NOT give fluid in established ATN — supportive only
Withhold nephrotoxins; adjust doses of renally cleared drugs
Treat hyperkalaemia, acidosis, fluid overload, sepsis
RRT — for AEIOU indications: refractory Acidosis, Electrolytes (K >6.5), Intoxications, Overload, Uraemic complications
Recovery over 7–21 days; sepsis delays recovery

Reveal

Special

Nephrotoxic ATN — spares basement membrane, targets whole PCT → good regeneration
Ischaemic ATN — focal rupture of tubular basement membrane → incomplete regeneration in those areas
Gross — enlarged kidney, pale necrotic cortex, congested medulla
Two oliguria mechanisms — (1) tubular damage → renin-angiotensin → afferent VC → ↓GFR; (2) debris blocks lumen → ↑intratubular pressure → fluid leak to interstitium → collapsed tubules
Non-oliguric AKI usually reflects a less severe renal insult (better prognosis); oliguria is the common early finding

Reveal

Rhabdomyolysis

C/P

Skeletal muscle injury releases myoglobin → nephrotoxic ATN ("crush syndrome")
Causes — trauma, compartment syndrome, excessive exertion (marathon runners), status epilepticus
Muscle toxins — statins, malaria/antimalarials, snake/insect venom
Dark brown / tea-coloured urine + oliguria + AKI

Reveal

Inves

Urine dipstick — positive for blood, but no RBCs on microscopy (myoglobin cross-reactivity)
Elevated markers — K↑, PO4↑, CPK↑↑ (creatine phosphokinase)
Serum myoglobin
Renal function — rising BUN/creatinine consistent with ATN
Assess for compartment syndrome — surgical review

Reveal

Mng

Aggressive IV fluid resuscitation — crystalloids to maintain urine output and flush myoglobin
Treat hyperkalaemia — insulin/dextrose, calcium gluconate for ECG changes
Fasciotomy — if compartment syndrome
Haemodialysis if severe AKI or refractory hyperkalaemia
Tubular epithelium regenerates with supportive care

Reveal

Special

Urine dipstick positive for blood but no RBCs on microscopy — pathognomonic for myoglobin/haemoglobin
Classic AKI arc — oliguric maintenance phase → recovery phase polyuria (>3 L/day) as tubules recover before concentrating ability

Reveal

Acute Kidney Injury (AKI)

C/P

Abrupt deterioration in renal function over hours–days, usually reversible
Acute symptoms — dyspnoea, N/V, diarrhoea
Common — 1 in 5 hospitalised adults, 1 in 3 hospitalised children; ~5% UK community admissions; sepsis (25%) or septic shock (50%)
3 anatomical categories — pre-renal (hypoperfusion), renal parenchymal, post-renal (obstruction)
Pre-renal causes — hypovolaemia (dehydration, haemorrhage), hypotension without hypovolaemia (cirrhosis, septic shock), low cardiac output (cardiac failure, cardiogenic shock)
Intrinsic (renal parenchymal) — 4 subtypes: ATN (80–90%), glomerular (acute RPGN), acute tubulointerstitial, vascular (vasculitis, accelerated hypertension, cholesterol embolism, HUS)
Post-renal — prostate disease (men) or bilateral ureteric obstruction (stones/tumours); hesitancy + frequency; palpable bladder + suprapubic dullness on exam
Assess volume status — hypovolaemia signs: low BP, rapid pulse, sunken eyes, collapsed neck veins

Reveal

Inves

Serum urea + creatinine + eGFR — stage per RIFLE/AKIN/KDIGO
Blood urea to creatinine ratio > 20:1 (urea:creatinine >40:1) — suggests pre-renal
Urine chemistry — FENa <1%, urine Na <10, urine osm >500 in pre-renal; opposite in intrinsic
Urinalysis — RBC casts (glomerulonephritis), free Hb/myoglobin, pigmenturia
Early biomarkers — KIM-1, NGAL rise within hours
Serum chemistry — U&E, Ca, PO4, albumin, ALP, urate; CBC, coagulation, blood cultures, nephrotoxic drug levels; immune profile if GN suspected
Ultrasound of abdomen + pelvis — mandatory to exclude obstruction; check bladder
Renal biopsy — indicated if unexplained urine abnormalities (proteinuria/haematuria), persistent ATN >4 weeks, unclear aetiology, suspected systemic disease
Acute vs chronic — kidneys normal size on US in AKI vs small in CKD (except diabetes, where CKD kidneys stay normal/large); previous creatinine normal; anaemia, high PTH, hyperphosphataemia and hypocalcaemia less common than in CKD

Reveal

Mng

Fluid balance — daily weights, lying/standing BP, intake/output; withhold nephrotoxins
Pre-renal — fluid challenge of 250 mL crystalloid; Plasmalyte or Ringer's lactate preferred over 0.9% saline (avoid hyperchloraemic acidosis)
Post-renal — urethral catheter + upper tract imaging; nephrostomy for upper tract obstruction
Intrinsic ATN — DO NOT give fluid once established; supportive
Treat hyperkalaemia, acidosis, pulmonary oedema, sepsis
Adjust drug doses daily; particular care with anticoagulants; salt + K restriction
RRT indications (all 5) — symptomatic uraemia (encephalopathy/pericarditis/tamponade), refractory hyperkalaemia, refractory pulmonary oedema, severe acidosis, drug removal (gentamicin, lithium, severe aspirin overdose)

Reveal

Special

Uncomplicated AKI mortality <5–10%; ITU + multi-organ failure 50–70%; sepsis-associated AKI much worse prognosis
Autoregulation defence — prostaglandins on afferent arteriole (blocked by NSAIDs); angiotensin II on efferent arteriole (blocked by ACE-i)

Reveal

Rhabdomyolysis

C/P

Skeletal muscle injury releases myoglobin → nephrotoxic ATN ("crush syndrome")
Causes — trauma, compartment syndrome, excessive exertion (marathon runners), status epilepticus
Muscle toxins — statins, malaria/antimalarials, snake/insect venom
Dark brown / tea-coloured urine + oliguria + AKI

Reveal

Inves

Urine dipstick — positive for blood, but no RBCs on microscopy (myoglobin cross-reactivity)
Elevated markers — K↑, PO4↑, CPK↑↑ (creatine phosphokinase)
Serum myoglobin
Renal function — rising BUN/creatinine consistent with ATN
Assess for compartment syndrome — surgical review

Reveal

Mng

Aggressive IV fluid resuscitation — crystalloids to maintain urine output and flush myoglobin
Treat hyperkalaemia — insulin/dextrose, calcium gluconate for ECG changes
Fasciotomy — if compartment syndrome
Haemodialysis if severe AKI or refractory hyperkalaemia
Tubular epithelium regenerates with supportive care

Reveal

Special

Urine dipstick positive for blood but no RBCs on microscopy — pathognomonic for myoglobin/haemoglobin
Classic AKI arc — oliguric maintenance phase → recovery phase polyuria (>3 L/day) as tubules recover before concentrating ability

Reveal

Tumour Lysis / Acute Hyperuricaemic Nephropathy

C/P

Complication of first cytotoxic/steroid treatment of lymphoproliferative tumours
Massive tumour cell lysis releases intracellular contents — URIC ACID, K, PO4
Uric acid crystal deposition in collecting ducts, pelvis, ureters → intrarenal + extrarenal obstruction → AKI

Reveal

Inves

Serum uric acid, K, PO4, Ca (may be low), LDH
Renal function — rising urea/creatinine
Ultrasound — may show extrarenal obstruction due to urate stones, or be unremarkable

Reveal

Mng

Allopurinol — prior to and throughout cytotoxic/radiotherapy treatment (prophylaxis)
Aggressive IV fluids — maintain high urine output
Sodium bicarbonate — alkalinise urine to solubilise urate
Febuxostat — if allopurinol not tolerated + eGFR >30
Rasburicase — recombinant urate oxidase; converts urate to soluble allantoin
Dialysis — severely oliguric/anuric patients

Reveal

Special

URIC ACID — highlighted release; primary cause of obstruction

Reveal

Acute Kidney Injury (AKI)

C/P

Abrupt deterioration in renal function over hours–days, usually reversible
Acute symptoms — dyspnoea, N/V, diarrhoea
Common — 1 in 5 hospitalised adults, 1 in 3 hospitalised children; ~5% UK community admissions; sepsis (25%) or septic shock (50%)
3 anatomical categories — pre-renal (hypoperfusion), renal parenchymal, post-renal (obstruction)
Pre-renal causes — hypovolaemia (dehydration, haemorrhage), hypotension without hypovolaemia (cirrhosis, septic shock), low cardiac output (cardiac failure, cardiogenic shock)
Intrinsic (renal parenchymal) — 4 subtypes: ATN (80–90%), glomerular (acute RPGN), acute tubulointerstitial, vascular (vasculitis, accelerated hypertension, cholesterol embolism, HUS)
Post-renal — prostate disease (men) or bilateral ureteric obstruction (stones/tumours); hesitancy + frequency; palpable bladder + suprapubic dullness on exam
Assess volume status — hypovolaemia signs: low BP, rapid pulse, sunken eyes, collapsed neck veins

Reveal

Inves

Serum urea + creatinine + eGFR — stage per RIFLE/AKIN/KDIGO
Blood urea to creatinine ratio > 20:1 (urea:creatinine >40:1) — suggests pre-renal
Urine chemistry — FENa <1%, urine Na <10, urine osm >500 in pre-renal; opposite in intrinsic
Urinalysis — RBC casts (glomerulonephritis), free Hb/myoglobin, pigmenturia
Early biomarkers — KIM-1, NGAL rise within hours
Serum chemistry — U&E, Ca, PO4, albumin, ALP, urate; CBC, coagulation, blood cultures, nephrotoxic drug levels; immune profile if GN suspected
Ultrasound of abdomen + pelvis — mandatory to exclude obstruction; check bladder
Renal biopsy — indicated if unexplained urine abnormalities (proteinuria/haematuria), persistent ATN >4 weeks, unclear aetiology, suspected systemic disease
Acute vs chronic — kidneys normal size on US in AKI vs small in CKD (except diabetes, where CKD kidneys stay normal/large); previous creatinine normal; anaemia, high PTH, hyperphosphataemia and hypocalcaemia less common than in CKD

Reveal

Mng

Fluid balance — daily weights, lying/standing BP, intake/output; withhold nephrotoxins
Pre-renal — fluid challenge of 250 mL crystalloid; Plasmalyte or Ringer's lactate preferred over 0.9% saline (avoid hyperchloraemic acidosis)
Post-renal — urethral catheter + upper tract imaging; nephrostomy for upper tract obstruction
Intrinsic ATN — DO NOT give fluid once established; supportive
Treat hyperkalaemia, acidosis, pulmonary oedema, sepsis
Adjust drug doses daily; particular care with anticoagulants; salt + K restriction
RRT indications (all 5) — symptomatic uraemia (encephalopathy/pericarditis/tamponade), refractory hyperkalaemia, refractory pulmonary oedema, severe acidosis, drug removal (gentamicin, lithium, severe aspirin overdose)

Reveal

Special

Uncomplicated AKI mortality <5–10%; ITU + multi-organ failure 50–70%; sepsis-associated AKI much worse prognosis
Autoregulation defence — prostaglandins on afferent arteriole (blocked by NSAIDs); angiotensin II on efferent arteriole (blocked by ACE-i)

Reveal

Acute Tubular Necrosis (ATN)

C/P

Final common pathway for many insults — accounts for 80–90% of intrinsic AKI
Ischaemic ATN — trauma, septicaemia, acute pancreatitis, hypotension/shock
Nephrotoxic ATN — poisons, drugs (aminoglycosides, contrast agents), organic solvents, myoglobin (rhabdo)
Four classical phases — onset (36 h) → oliguric (few days–3 weeks, marked oliguria + uraemia) → diuretic (polyuria >3 L/day) → recovery (weeks); usually partial residual impairment

Reveal

Inves

Urea/creatinine rising over days
Urine — muddy brown granular casts, renal tubular epithelial cell casts
Urine Na > 20, FENa >1%, urine osm <350 — distinguishes from pre-renal
Ultrasound — normal or enlarged kidneys (rule out post-renal)
Renal biopsy if persistent >4 weeks or unclear cause

Reveal

Mng

DO NOT give fluid in established ATN — supportive only
Withhold nephrotoxins; adjust doses of renally cleared drugs
Treat hyperkalaemia, acidosis, fluid overload, sepsis
RRT — for AEIOU indications: refractory Acidosis, Electrolytes (K >6.5), Intoxications, Overload, Uraemic complications
Recovery over 7–21 days; sepsis delays recovery

Reveal

Special

Nephrotoxic ATN — spares basement membrane, targets whole PCT → good regeneration
Ischaemic ATN — focal rupture of tubular basement membrane → incomplete regeneration in those areas
Gross — enlarged kidney, pale necrotic cortex, congested medulla
Two oliguria mechanisms — (1) tubular damage → renin-angiotensin → afferent VC → ↓GFR; (2) debris blocks lumen → ↑intratubular pressure → fluid leak to interstitium → collapsed tubules
Non-oliguric AKI usually reflects a less severe renal insult (better prognosis); oliguria is the common early finding

Reveal

Tumour Lysis / Acute Hyperuricaemic Nephropathy

C/P

Complication of first cytotoxic/steroid treatment of lymphoproliferative tumours
Massive tumour cell lysis releases intracellular contents — URIC ACID, K, PO4
Uric acid crystal deposition in collecting ducts, pelvis, ureters → intrarenal + extrarenal obstruction → AKI

Reveal

Inves

Serum uric acid, K, PO4, Ca (may be low), LDH
Renal function — rising urea/creatinine
Ultrasound — may show extrarenal obstruction due to urate stones, or be unremarkable

Reveal

Mng

Allopurinol — prior to and throughout cytotoxic/radiotherapy treatment (prophylaxis)
Aggressive IV fluids — maintain high urine output
Sodium bicarbonate — alkalinise urine to solubilise urate
Febuxostat — if allopurinol not tolerated + eGFR >30
Rasburicase — recombinant urate oxidase; converts urate to soluble allantoin
Dialysis — severely oliguric/anuric patients

Reveal

Special

URIC ACID — highlighted release; primary cause of obstruction

Reveal

Practice exam

Timed, 60 seconds a question, drawn from every lecture you've done.

When something fails

Something didn't finish

This stage did not finish. You can retry it without losing what already ran.

Other screens

404

WOAH, the Genie doesn’t know where you’re going, mate

Click home to go back home

Server error

The Genie’s getting constipated, man, give him a minute (or lactulose lol)

Window too narrow

Come on, give the Genie some space. Widen the window

Account menu

1 · Definition ?

2 · Classification — RIFLE/AKIN/KDIGO ?

3 · Epidemiology?

4 · Approaching AKI?

5 · Pre-renal?

6 · Pre-renal or renal??

7 · Management of pre-renal?

8 · Post-renal?

9 · Renal parenchymal?

10 · Pathogenesis of ATN?

11 · Clinical picture?

12 · Emergency investigation?

13 · Investigations?

14 · Acute or chronic??

15 · Management?

16 · RRT?

17 · Rhabdomyolysis + contrast?

18 · Tumour lysis + hyperuricaemic nephropathy?

19 · Hepatorenal + Outcome?

One last yap: connect the dots

You covered:

Still missing:

Flashcards

All done, doc

PERFECTOMONDO

Electrolyte Disorders

Hypernatraemia

Hyponatraemia

Hypokalaemia

Hyperkalaemia

Acute Renal Injury

Acute Tubular Necrosis (ATN)

Rhabdomyolysis

Acute Kidney Injury (AKI)

Acute Tubular Necrosis (ATN)

Rhabdomyolysis

Acute Kidney Injury (AKI)

Rhabdomyolysis

Tumour Lysis / Acute Hyperuricaemic Nephropathy

Acute Kidney Injury (AKI)

Acute Tubular Necrosis (ATN)

Tumour Lysis / Acute Hyperuricaemic Nephropathy

Looks like a room full of people who LIKE HAVING 400K IN DEBT

WOAH

1 · Definition

2 · Classification — RIFLE/AKIN/KDIGO

3 · Epidemiology

4 · Approaching AKI

5 · Pre-renal

6 · Pre-renal or renal?

7 · Management of pre-renal

8 · Post-renal

9 · Renal parenchymal

10 · Pathogenesis of ATN

11 · Clinical picture

12 · Emergency investigation

13 · Investigations

14 · Acute or chronic?

15 · Management

16 · RRT

17 · Rhabdomyolysis + contrast

18 · Tumour lysis + hyperuricaemic nephropathy

19 · Hepatorenal + Outcome