Mednotes

Renal Concept checklist

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Renal: Concept Checklist

Concepts covered across the module lectures, grouped by lecture. Tick each once you can explain it from memory.

L1 Introduction to the Renal Module (18 May) L1 Renal Introduction to the Renal Module

  • Quantitative renal physiology: renal blood flow, filtered volume and sodium load, urine output, segmental reabsorption
  • Structure of the nephron, renal corpuscle and the three-layer glomerular filtration barrier
  • Starling forces across the glomerular capillary and why small perfusion changes alter GFR
  • Mechanisms preserving GFR: myogenic response, tubuloglomerular feedback, RAAS and sympathetic control; shifted and lost autoregulation in hypertension and CKD
  • Tubular sodium handling: basolateral Na+/K+-ATPase and apical entry mechanisms by segment; thick ascending limb and frusemide action
  • Countercurrent concentrating mechanism and urea recycling
  • Aquaporins in the kidney and AVP/V2-mediated AQP2 insertion
  • Urinalysis for kidney disease: dipstick, microscopy, glomerular haematuria
  • Nephrotic vs nephritic syndromes as a continuum
  • Acute post-infectious glomerulonephritis: presentation, histology, and pathophysiology of oliguria, hypertension and oedema
  • Nephrotic syndrome: podocyte injury and oedema via oncotic and hydrostatic (sodium retention) arms
  • Diabetic kidney disease: macro- vs microvascular disease and natural history from increased GFR to end stage renal disease
  • CKD epidemiology in NZ and ethnic inequities, KDIGO GFR/albuminuria risk classification, mortality by eGFR, extrarenal manifestations
  • Kidney replacement therapy in NZ: incidence, ethnicity, causes, comorbidities, dialysis vs transplantation trends

L2 Physiology 1 (20 May) L2 Renal Physiology 1

  • Four functions of the kidney: excretion, homeostasis, hormone production, metabolism
  • Renal hormones: erythropoietin (anaemia in CKD) and calcitriol via 1-alpha-hydroxylase (renal osteodystrophy)
  • Renal roles in gluconeogenesis, ammonia synthesis, acid-base, fluid and electrolyte balance
  • Interpreting a chronic renal failure presentation from its clinical and biochemical features
  • Structure of the nephron: cortical vs juxtamedullary nephrons, tubular segments and accompanying vasculature
  • Filtration, reabsorption and secretion, and the net excretion equation; division of labour along the nephron
  • Glomerulus and juxtaglomerular apparatus structure
  • The three layers of the filtration barrier and size and charge selectivity
  • Determinants of GFR, Starling forces and net filtration pressure; pressure profile along renal vessels
  • GFR normal values and variation; renal plasma flow, filtration fraction and filtered load
  • Clearance: formula, and why creatinine or inulin clearance estimates GFR

L3 Physiology 2 (21 May) L3 Renal Physiology 2

  • Map of nephron processes: filtration, bulk reabsorption, medullary gradient, fine-tuning of electrolytes and water
  • Renal blood supply: proportion of cardiac output, cortical vs medullary distribution, and the arteriole-capillary-arteriole arrangement
  • Effects of afferent vs efferent arteriolar constriction and dilation on glomerular pressure and GFR
  • Autoregulation of RBF and GFR: myogenic mechanism and tubuloglomerular feedback via the macula densa and juxtaglomerular apparatus
  • Extrinsic control of renal blood flow: sympathetic nerves, angiotensin II (efferent predominance), prostaglandins; why NSAIDs cause renal ischaemia
  • Solutes that are reabsorbed only, secreted only, or both
  • Paracellular vs transcellular transport across tubular epithelium
  • Proximal tubule bulk reabsorption, Na+-driven secondary active transport, and secretion of organic acids and drugs
  • Glucose handling: complete reabsorption normally, and glucose in urine when the filtered load exceeds reabsorptive capacity (diabetes mellitus)
  • Proximal bicarbonate reclamation via H+ secretion and carbonic anhydrase
  • Thick ascending limb: water impermeability, NaK2Cl transport and generation of the hyperosmotic medullary gradient
  • Distal tubule and collecting duct fine-tuning under aldosterone and ADH; daily Na+ and water handling along the nephron

L4 Physiology 3_4 (22 May) L4 Renal Physiology 3_4

  • Principles of water reabsorption: bulk isotonic proximal reabsorption coupled to sodium, fine-tuning in the collecting duct under ADH
  • Loop of Henle and the hyperosmotic medullary gradient; role of urea and countercurrent exchange in the vasa recta
  • Body water compartments: total body water by sex, ICF vs ECF, interstitial vs plasma volumes
  • Ionic composition of ECF vs ICF
  • Daily water balance: sources of intake and routes of loss, urine as the adjustable term
  • Why water must be regulated: osmolarity, fluid shifts between ECF and ICF, and cell volume
  • Osmoregulatory feedback loop: hypothalamic osmoreceptors, ADH, thirst
  • ADH synthesis and release, stimuli (osmolarity vs blood volume thresholds) and actions
  • Mechanism of ADH action via V2 receptor, cAMP/PKA and AQP2 insertion
  • Limits of urine concentration and flow
  • Thirst: triggers and the dipsogenic threshold relative to ADH regulation
  • Collecting duct behaviour with vs without ADH; mechanisms of diuresis (absent ADH, disrupted gradient, osmotic diuresis)
  • Applying water homeostasis to cases: water excess, absent ADH or ADH response, inappropriately concentrated urine with hyponatraemia, osmotic diuresis in diabetes

L5 Physiology 5 (25 May) L5 Renal Physiology 5

  • Normal ECF pH and H+ concentration, limits compatible with life, and why pH must be controlled
  • Scale of the daily acid load and the roles of buffering and excretion
  • CO2 as a volatile acid: haemoglobin buffering in transit and ventilation; respiratory acidosis vs alkalosis
  • Non-volatile acids: sources, net endogenous acid production, whole-body buffering (bicarbonate, protein, phosphate, bone)
  • Renal bicarbonate reclamation: sites and proximal tubule mechanism via NHE3 and carbonic anhydrase
  • Renal net acid excretion and generation of new bicarbonate via titratable acid (phosphate) and ammonium (glutamine metabolism)
  • Fate of a non-volatile acid from production to excretion
  • Henderson-Hasselbalch equation, and renal vs respiratory control of its components
  • Proximal vs distal renal tubular acidosis: defects, causes and case features
  • The four primary acid-base disturbances and their causes

L6 Physiology 6 (and stuff from 5 (25 May) L6 Renal Physiology 6 (and stuff from 5

  • Henderson-Hasselbalch 20:1 ratio and restoring pH by changing the other variable
  • Respiratory compensation of metabolic disturbances and renal compensation of respiratory disturbances
  • How the kidney adjusts bicarbonate handling, titratable acid and ammonium excretion in acidosis vs alkalosis
  • Causes of metabolic alkalosis
  • Anion gap: calculation, normal range, and what it estimates
  • Normal vs high anion gap metabolic acidosis: causes and mechanism of electroneutrality (chloride vs unmeasured anions)
  • Metabolic alkalosis from nasogastric losses and paradoxical aciduria when volume retention takes priority
  • Diabetic ketoacidosis: acid-base interpretation, anion gap, and why plasma K is high despite a whole-body deficit
  • Potassium roles, distribution between ICF and ECF, and daily turnover
  • Internal potassium balance: factors shifting K into or out of cells (insulin, adrenaline, aldosterone, pH, osmolarity, exercise)
  • External potassium balance: renal handling along the nephron and distal secretion vs reabsorption

L7 Histology 1 (27 May) L7 Renal Histology 1

  • Low-power kidney architecture: cortex vs medulla, renal lobe, and why renal corpuscles identify the cortex
  • Spatial layout of the nephron segments
  • Embryological origin of the renal corpuscle and the dual origin of the kidney (ureteric bud vs metanephric mesenchyme)
  • Histological components of the renal corpuscle, vascular vs urinary pole, and role of arteriolar diameter in glomerular pressure
  • The filtration barrier on EM: fenestrated endothelium, type IV collagen GBM, podocyte foot processes and slits
  • Proximal convoluted tubule histology and how brush border, basolateral interdigitations and mitochondria relate to function
  • Loop of Henle segments: epithelial type and transport function of pars recta, thin limbs and thick ascending limb

L9 Glomerulonephritis (20 May) L9 Renal Glomerulonephritis

  • Normal glomerular capillary wall structure and barrier properties; occluded loops in nephritic vs foot process effacement in nephrotic disease
  • Antigen categories initiating GN: exogenous, exogenous self, endogenous glomerular antigens
  • Humoral and cellular mechanisms of immune glomerular injury
  • Complement pathways converging on C3, and effector products C5a and C5b-9
  • Innate and adaptive immune limbs in glomerular injury
  • Routes of deposit formation (circulating complex trapping, in situ planted antigen, in situ endogenous antigen) and determinants of their consequences
  • Endothelial proliferative vs epithelial podocyte patterns of glomerular injury
  • Post-streptococcal GN: pathogenesis, histology (endocapillary proliferation, subepithelial humps), GAS virulence factors and emm types
  • Post-streptococcal GN in NZ: epidemiology by ethnicity and deprivation, clinical and laboratory features (haematuria, low C3), outcomes
  • Membranous GN: nephrotic presentation, histology, anti-PLA2R/THSD7A IgG4, why it is non-inflammatory, C5b-9 podocyte injury and progression, natural history
  • Rapidly progressive (crescentic) GN: presentation, anti-GBM linear IgG staining, phases of glomerular inflammation
  • Clinical classification of GN presentations
  • Pathophysiology of oedema in nephrotic syndrome (including plasmin-activated ENaC) and of acute nephritic syndrome; nephritic urinalysis findings

L10 Physiology 7 (27 May) L10 Renal Physiology 7

  • Definition and features of acute kidney injury
  • Classification of AKI into pre-renal, intra-renal and post-renal, with mechanisms and causes of each
  • Acute tubular necrosis: proportion of intrinsic AKI, ischaemic vs nephrotoxic causes, pathogenesis theories, three phases
  • Ischaemic ATN mechanism and morphology
  • Applying AKI physiology to post-operative ATN after ruptured AAA repair
  • Why creatinine clearance no longer estimates GFR once tubules are damaged
  • Metabolic acidosis and hyperkalaemia in ATN due to loss of tubular function
  • Recovery phase of ATN: regenerating immature epithelium, inability to concentrate urine, osmotic diuresis and risk of volume and electrolyte depletion

L11 Histology 2 (29 May) L11 Renal Histology 2

  • Distal convoluted tubule histology and why it lacks microvilli
  • Juxtaglomerular apparatus: macula densa, lacis cells and juxtaglomerular granular cells, and their roles
  • Collecting tubule and duct: principal vs intercalated cell functions and change from cuboidal to columnar epithelium
  • Ducts of Bellini opening at the renal papilla and transition to transitional epithelium
  • Ureter wall layers and the extra muscle layer of its distal third; bladder detrusor muscle
  • Transitional epithelium: umbrella cells, plaques and vesicles enabling distensibility and impermeability
  • Epithelial changes along the male urethra from bladder to external orifice

L12 Acute kidney injury (AKI) (29 May) L12 Renal Acute kidney injury (AKI)

  • Definition of AKI: creatinine rise and oliguria criteria
  • LION classification of AKI causes: low perfusion, inflammatory/immune, obstructive, nephrotoxic
  • Glomerular pressures and renal autoregulation: myogenic response, tubuloglomerular feedback steps at low vs high NaCl, RAAS and SNS
  • Vasoconstrictor/vasodilator balance determining GFR; angiotensin II in the stress response
  • Limits of autoregulation: impaired reactivity with age, CKD and vascular disease; MAP threshold and relative hypotension in hypertensive patients
  • Haemodynamic insults and drugs reducing renal compensation, and the triple whammy
  • Why the medulla is vulnerable to ischaemic ATN: oxygen gradient, target segments, endothelial injury cascade, continuum and repair of tubular injury
  • AKI from volume depletion with an ileostomy: severe acidosis, hyperkalaemia and its ECG progression, treatment, delayed creatinine fall
  • Post-renal AKI: investigation, mechanism via raised intracapsular pressure, management and post-obstructive diuresis; recovery-phase risks
  • Cardiorenal syndrome: arterial underfilling and venous congestion pathways; management of congestive heart failure
  • Clinical assessment of AKI: volume status (postural BP, JVP, weight), urine osmolality and sodium in low perfusion vs ATN, assessment for obstruction and intrinsic causes
  • Management of AKI: the 3 Vs for hypoperfusion, harms of fluid overload, relieving obstruction, treating renal causes, general care, indications for dialysis
  • Outcomes of AKI: mortality by organ involvement, structural outcome by severity, increased risk of CKD and cardiovascular disease

L13 Physiology 8 (3 Jun) L13 Renal Physiology 8

  • Definition and key features of CKD, common causes, and heterogeneous function of remaining nephrons
  • Distinguish acute from chronic renal failure
  • Staging of chronic renal failure by GFR and the features that emerge at each stage
  • Consequences of nephron loss grouped by decreased excretion, decreased biosynthesis and altered metabolism
  • Organ system involvement in CKD and its mechanisms
  • Water handling by hypertrophied nephrons: inability to concentrate or dilute urine, polyuria and nocturia
  • Sodium handling in CKD: reduced fractional reabsorption and the possibility of salt wasting or salt retention
  • Potassium handling in CKD and the tendency to hyperkalaemia
  • Urea and creatinine handling in CKD: why plasma levels rise non-linearly as GFR falls, and the time course after an abrupt GFR fall
  • Mechanisms of metabolic acidosis in CKD
  • Calcium, phosphate and bone in CKD: hyperphosphataemia, reduced vitamin D activation, secondary hyperparathyroidism, renal osteodystrophy, metastatic calcification
  • Mechanisms of hypertension in CKD, and oedema in CKD (volume-driven, unlike nephrotic syndrome)

L14 Hypertension (4 Jun) L14 Renal Hypertension

  • Initial assessment of hypertension: confirming with ambulatory BP monitoring, cuff error, and screening for secondary causes (sleep apnoea, renal, endocrine, renovascular)
  • Renal artery stenosis (fibromuscular hyperplasia): hypokalaemia with high renin and high aldosterone, diagnosis and cure by angioplasty
  • Cortical collecting duct principal and intercalated cells, and how aldosterone causes hypokalaemia and metabolic alkalosis
  • Primary hyperaldosteronism: suppressed renin with high aldosterone, adrenal imaging, spironolactone vs surgery
  • Mechanisms of aldosterone-driven hypertension and spironolactone action
  • Pathophysiology of essential hypertension: TPR, endothelial dysfunction, polygenic renal component, definition of elevated BP
  • Salt and the kidney: evolutionary mismatch, NZ salt intake and sources, WHO target
  • Guyton pressure-natriuresis hypothesis and the right-shifted curve in hypertension
  • Aldosterone, endothelial ENaC and salt-sensitive vascular stiffness
  • Vascular pathology in hypertension: arteriosclerosis vs atherosclerosis, pulse wave reflection and augmentation index, end-organ effects of stiffness
  • Hypertension in CKD: prevalence, contributing factors, renal histology, loss of autoregulation and progressive nephropathy
  • Expected creatinine rise after starting an ACEI or ARB due to efferent dilation, vs true AKI or renal artery stenosis
  • BP targets (SPRINT), salt restriction, proteinuria as a risk marker, lower targets and maximal ACEI/ARB dosing in proteinuric kidney disease, when to start drug therapy

L15 Chronic Kidney Disease (5 Jun) L15 Renal Chronic Kidney Disease

  • Diabetic nephropathy case: staging (G3b A3), cardiovascular and renal risk calculation, constellation of diabetic complications
  • Definition of CKD and KDIGO CGA staging by eGFR and albuminuria categories; risk heat map and monitoring frequency
  • CKD epidemiology and risk factors in NZ including ethnic inequities; who to screen
  • Why CKD progresses: secondary haemodynamic and metabolic factors, glomerular hypertrophy and secondary FSGS as the final common pathway
  • Management across the CKD trajectory: lifestyle, drugs for progression and cardiovascular risk, comorbidity management, transition to KRT and supportive care
  • Hypertension in CKD: BP targets, ACEI/ARB as first choice and the expected GFR dip, roles of SGLT2i, diuretics, CCBs and beta-blockers; RENAAL and SPRINT evidence
  • Proteinuria as the strongest predictor of progression; lower BP target, ACEI/ARB even if normotensive, proteinuria targets, uACR testing
  • SGLT2 inhibitor trials in CKD and heart failure (DAPA-CKD, EMPA-KIDNEY, DAPA-HF) and benefit regardless of diabetes
  • The four pillars (RASi, SGLT2i, finerenone, GLP-1 RA): mechanisms and combination benefit; standard of care and proven risk strategies
  • CKD and cardiovascular disease: risk rising with falling eGFR, mechanisms of cardiac injury (volume, FGF23/Klotho, calcification, angiotensin II), LVH
  • Extra-renal manifestations framework; anaemia of CKD: mechanism and treatment (iron, avoiding unnecessary tests and transfusion, EPO targets)
  • CKD-mineral bone disorder: normal phosphate/PTH/FGF23/vitamin D regulation and the stepwise derangement in CKD including Klotho loss
  • Biochemical and radiological phenotype of secondary hyperparathyroidism, vascular calcification, tertiary hyperparathyroidism and calciphylaxis
  • Management of secondary hyperparathyroidism: phosphate restriction and binders, calcitriol, calcimimetics, bicarbonate, parathyroidectomy
  • Metabolic acidosis in CKD and benefits of bicarbonate
  • Kidney replacement therapy options, when dialysis starts, transplantation and organ donation; NZ kidney failure data and ethnic inequities

L19 Radiology _ Medicine (10 Jun) L19 Renal Radiology _ Medicine

  • Differential diagnosis of haematuria and clinical clues (painless haematuria in older smokers, colicky loin-to-groin pain)
  • Renal trauma: FAST vs contrast CT, CT findings, AAST renal injury grades I to V, post-traumatic renovascular hypertension
  • Nuclear medicine studies: MAG3 renogram, Tc99-MDP bone scan, SPECT-CT, PSMA PET-CT, and what each tracer shows
  • Renal cell carcinoma: presentation, CT staging with pulmonary and bone metastases, clear cell vs papillary pathology
  • Urinary tract calculi: presentation, KUB and CT findings, secondary signs of obstruction, calcium oxalate stones
  • Polycystic kidney disease: presentation, CT and ultrasound appearance, gross pathology
  • Prostate disease: MRI of prostate cancer, staging, pathology of cancer vs BPH vs chronic prostatitis
  • Clinical algorithm for investigating visible vs non-visible haematuria, including imaging, cystoscopy and cytology
  • Criteria for nephrology referral and monitoring for nephrological vs urological causes; risk factors for significant urological disease

L20 RENAL CLINICAL DAY (17 Jun) L20 Renal RENAL CLINICAL DAY

  • Renal colic: presentation, differential, CT-KUB as the diagnostic test, stone types and frequencies, mechanism of stone formation
  • Acute management of renal colic (analgesia, alpha blocker) and definitive treatment by stone site and size; CARI acute pathway
  • Stone investigations and prevention: fluids, diet (calcium, salt, oxalate, animal protein), allopurinol, potassium citrate, thiazides
  • UTI organisms in community vs hospital, uncomplicated UTI treatment options, and why urinary alkalinisation undermines nitrofurantoin
  • Indications and regimens for UTI prophylaxis; topical oestrogen; lack of evidence for cranberry
  • Deciding whether to treat bacteriuria in different patients, and trimethoprim-related creatinine rise
  • Recurrent Proteus UTI and struvite staghorn calculi
  • Approach to haematuria: urological vs nephrological, investigation by age, risk factors for urological malignancy, monitoring and referral criteria
  • Synpharyngitic haematuria with proteinuria as glomerulonephritis until proven otherwise
  • IgA nephropathy: mesangial pattern, presentations by age, four-hit hypothesis (galactose-deficient IgA1), natural history and where therapies act
  • Hyponatraemia as a water disorder: framework of volume assessment, plasma and urine osmolality; SIADH causes and management
  • Cardiorenal syndrome: non-osmotic AVP release, salt and water retention sequence, dual haemodynamic pathways, fluid overload sustaining AKI
  • Managing acute heart failure with AKI: decongestion, why ACEI/ARB help despite low BP, identifying the cause of rising creatinine
  • Diabetic kidney disease risk: effect of ethnicity and smoking on calculated risk; drug choices, SGLT2 inhibitor properties; foundations and pillars of therapy with combination effects

L21 In-course Renal essay feedback (15 Jul) L21 Renal In-course Renal essay feedback

  • Diabetic nephropathy with nephrotic-range proteinuria: interpreting presentation, hypertension from Na+ retention, cardiomegaly without heart failure
  • Examination findings for macrovascular and microvascular complications of diabetes
  • SGLT2 inhibitor mechanism via tubuloglomerular feedback, expected effects, sick day rules, and practical checklist for starting in T2DM with CKD
  • ARBs in diabetic kidney disease: systemic and kidney-specific actions
  • Interpreting an expected eGFR fall after starting SGLT2i and ARB as a beneficial reduction in intraglomerular pressure
  • AKI after cardiac arrest: neurohormonal pathway to salt and water retention, urine biochemistry, acidosis and hyperkalaemia
  • Frusemide: NKCC2 blockade, protein binding and tubular secretion as a weak organic anion, effect on paracellular cation transport
  • Secondary prevention medications after MI with AKI and their rationale
  • Post-streptococcal GN: confirmatory investigations, histology, immune complex and complement pathogenesis, complement regulators, treatment
  • Advanced CKD: interpreting anaemia, hyperuricaemia, hypoalbuminaemia and HbA1c; CKD-MBD pathogenesis; management of each abnormality
  • Pre-renal AKI from ileostomy losses on CKD: diagnosis, acidosis and hyperkalaemia mechanisms, immediate fluid management, avoiding ACEI/ARB acutely, long-term plan

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