Renal A&P and scanning

Kidney position and size

10-12 cm long, 3 cm thick, 5-7 cm wide; lie posteriorly between T12 and L3, partly protected by ribs 11 and 12, retroperitoneal; right kidney sits slightly lower due to the liver above it; adrenal glands sit on top of each kidney

Kidney filtration capacity

Filter about 150 L of blood per day; each kidney has about 1 million nephrons; best view for nuclear medicine renal imaging is posterior

Ureter anatomy

25-30 cm long, thick-walled, retroperitoneal; peristalsis (plus pressure and gravity) moves urine; diameter 1-10 mm; enter the posterior bladder wall, not the top

Ureteric valve mechanism

A filling bladder compresses the ureter openings as a physiological valve to prevent backflow; if it fails, microbes can travel up to infect the kidneys

Three normal ureteric constrictions

Pelvi-ureteric junction (PUJ), pelvic brim (crossing the iliac vessels), uretero-vesical junction (UVJ) — the commonest obstruction sites

Kidney protective layers (outer to inner)

Renal fascia (outer, anchors kidney), adipose capsule (middle, fat, protects from trauma), renal capsule (inner, gives kidney its shape)

Renal cortex vs medulla

Cortex is the outer zone of functional tissue, holding about 85% of nephrons; medulla is the inner zone containing renal pyramids and papillae (cortex between pyramids = renal columns; pyramid plus overlying cortex = renal lobe)

Urine collecting system path

Minor calyces to major calyces to renal pelvis to ureter

Kidney hormone functions

Calcitriol (active vitamin D, calcium homeostasis), erythropoietin (red cell production), renin (starts RAAS)

Other kidney functions

Gluconeogenesis during fasting (mainly proximal tubule); blood pH regulation (excrete H+, conserve bicarbonate); ionic composition (Na+, K+, Ca2+, Cl-, phosphate); blood volume/pressure (water conservation, RAAS); waste excretion; blood osmolarity kept near 300 mOsm/L

Nitrogenous wastes

Urea and ammonia (from amino acid deamination), creatinine (from muscle creatine phosphate), uric acid (from nucleic acids), urobilin (from haemoglobin); blood creatinine is used to assess kidney function

Renal corpuscle

The glomerulus (capillary ball) plus the glomerular (Bowman's) capsule; filtrate enters the capsular space

Renal tubule order

Proximal convoluted tubule (PCT) to nephron loop (loop of Henle) to distal convoluted tubule (DCT); several DCTs drain into one collecting duct, then papillary ducts, then minor calyces

Nephron location

The corpuscle and both convoluted tubules are in the cortex; the loop dips into the medulla; 85% are cortical nephrons with short loops, doing most of the work

Three nephron functions

Glomerular filtration, tubular reabsorption (back to blood), tubular secretion (blood to filtrate)

Renal blood flow path

Renal artery to segmental arteries to interlobar arteries (through renal columns) to arcuate arteries (around pyramids) to cortical radiate arteries to afferent arteriole to glomerulus to efferent arteriole to peritubular capillaries (cortex) and vasa recta (medulla) to cortical radiate veins to arcuate veins to interlobar veins to a single renal vein to the inferior vena cava (no segmental veins)

Glomerular filtration membrane layers

1) Capillary endothelium — fenestrated, about 50x more porous than ordinary capillaries, blocks blood cells; 2) basement membrane — gel-like mesh blocking larger plasma proteins; 3) epithelium (podocytes) — interlocking pedicels with filtration slits that allow water, glucose, amino acids, urea, ions, and very small proteins through

Filtrate and GFR values

Filtrate about 180 L/day (men), 150 L/day (women); GFR averages 125 mL/min (men), 105 mL/min (women); about 99% is reabsorbed so only 1-2 L becomes urine

Pressures driving filtration (NFP)

Glomerular blood hydrostatic pressure (GBHP, 55 mmHg, promotes filtration) minus blood colloid osmotic pressure (BCOP, 30 mmHg) and capsular hydrostatic pressure (CHP, 15 mmHg), both opposing filtration; NFP = 55 - (30+15) = 10 mmHg; filtration stops if GBHP falls to about 45 mmHg

Juxtaglomerular (JG) apparatus

Located between the DCT and afferent arteriole; made of macula densa cells (DCT wall), juxtaglomerular/granular cells (afferent arteriole wall), and extraglomerular mesangial cells

Renal autoregulation

Keeps renal blood flow and GFR constant at mean arterial pressure 80-180 mmHg via the myogenic mechanism (raised pressure stretches the afferent arteriole, triggering contraction that lowers GFR, within seconds) and tubuloglomerular feedback (high GFR increases Na+/Cl- delivery to the macula densa, reducing nitric oxide release and causing afferent vasoconstriction)

Neural control of GFR

Sympathetic fibres release norepinephrine acting on afferent arteriole alpha-1 receptors, causing vasoconstriction and lowering GFR (e.g. during intense exercise or hypovolaemic shock) to conserve blood volume

Angiotensin II effect on GFR

Triggered by low blood pressure/volume via renin; constricts afferent and efferent arterioles and contracts mesangial cells, lowering GFR, reducing urine output, and conserving volume

ANP effect on GFR

Triggered by a large rise in blood volume stretching the atria; relaxes mesangial cells, increasing filtration surface area, raising GFR, increasing urine output, and lowering volume/pressure

Tubular reabsorption routes

Paracellular (passive, between tubule cells through tight junctions, leakiest in the PCT) and transcellular (active, through tubule cells via channels/transporters like Na+/K+ ATPase and sodium-glucose cotransporters)

Obligatory vs facultative water reabsorption

Obligatory (~90%) occurs by osmosis following solutes mainly in the PCT and loop of Henle; facultative (~10%) occurs in the last part of the DCT and collecting duct, controlled by ADH inserting aquaporin-2 into the apical membrane

Tubular secretion

Active, one-way transport of wastes, drugs, and excess ions from peritubular capillaries into tubular fluid, mainly in the PCT, DCT, and collecting ducts, via organic anion/cation transporters (mostly PCT)

Angiotensin II hormonal action

Triggered by low blood volume/pressure via renin; increases Na+/H+ antiporter activity in the PCT (more Na+ and water reabsorbed), stimulates thirst and sodium appetite, raising blood volume and pressure

Aldosterone hormonal action

Triggered by rising angiotensin II or plasma K+; increases Na+/K+ pumps and Na+ channels in DCT/collecting duct principal cells, increasing K+ secretion and Na+/water reabsorption

ADH hormonal action

Triggered by rising blood osmolarity or falling volume; inserts aquaporin-2 in the DCT/collecting duct, increasing water reabsorption

ANP hormonal action

Triggered by a large rise in blood volume (atrial stretch); suppresses Na+/water reabsorption and inhibits aldosterone/ADH, increasing urine output and lowering volume/pressure

Triggers for renin release

Beta-1 adrenergic receptors on JG cells (sympathetic activity), intrarenal baroreceptors sensing a fall in afferent arteriole pressure, and the macula densa sensing very low Na+/Cl- delivery

RAAS steps

Reduced renal blood flow triggers JG cells to release renin; renin converts liver-made angiotensinogen to angiotensin I; ACE (mainly in lung capillaries) converts it to angiotensin II; angiotensin II causes systemic vasoconstriction, increases PCT Na+/water reabsorption, lowers GFR, and stimulates aldosterone; aldosterone increases Na+ reabsorption and K+ secretion, with ADH further increasing water reabsorption; blood volume and pressure return toward normal

Kidney Pathologies

Congenital renal anomalies

Renal agenesis (inadequate formation, single or no kidney), renal hypoplasia (abnormally small, fewer nephrons but normal form), renal dysplasia (abnormally formed, function often impaired), horseshoe kidney (joined into one arched kidney, usually normal function but UTI/stone/obstruction risk), ureteral obstruction (often at PUJ or UVJ), vesicoureteral reflux (valve fails, urine flows back, causing recurrent UTIs and scarring), duplex collecting system (two ureters draining one kidney)

Urinary tract obstruction causes

Congenital abnormality, urethral stricture (scar tissue), prostate enlargement (compresses the urethra), kidney stones (crystallised calcium/uric acid); most likely at the PUJ, pelvic brim, or UVJ

Hydronephrosis

Swelling of the kidney from dilation of the renal pelvis and calyces due to obstructed urine flow; severe cases can cause renal failure

UTI (urinary tract infection)

Most commonly caused by E. coli, also mycoplasma/chlamydia; more common in females due to a shorter urethra; symptoms include painful/burning urination, urgency, frequency, smelly urine, low back pain, bedwetting

UTI site classification

Urethritis (urethra inflamed), cystitis (bladder inflamed), pyelonephritis (kidney inflamed); chronic pyelonephritis causes scarring that impairs kidney function

Renovascular hypertension

Caused by progressive renal artery stenosis, usually from atherosclerosis; one of the commonest causes of secondary hypertension; stenosis lowers afferent arteriole pressure, so JG cells release renin, raising systemic blood pressure via angiotensin II despite normal systemic pressure

Angiotensin II's dual role in renal artery stenosis

It normally lowers GFR, but in stenosis it constricts both afferent and efferent arterioles to help restore glomerular pressure and maintain GFR, even though overall renal blood flow to that kidney stays reduced; chronic ischaemia leads to kidney atrophy, nephron loss, and fibrosis (ischaemic nephropathy)

Renal failure consequences

Oedema (salt/water retention), metabolic acidosis (can't excrete acids), raised urea and creatinine (impaired waste excretion), high potassium (can cause cardiac arrest), anaemia (less erythropoietin), low calcium absorption (can't make calcitriol)

Acute vs chronic renal failure

Acute (AKI) is an abrupt decrease/stop in function with most patients recovering fully (causes

Chronic renal failure by cause

Pre-renal (prolonged reduced blood flow, e.g. dehydration, heart failure, bilateral renal artery stenosis), renal/intrinsic (direct kidney damage, e.g. glomerulonephritis, diabetic nephropathy, hypertension), post-renal (outflow obstruction, e.g. stones, tumours, enlarged prostate)

Chronic kidney disease staging (3-stage model)

1) Diminished renal reserve — up to 75% of nephrons lost, usually asymptomatic; 2) Renal insufficiency — over 75% lost, GFR falls, urea/creatinine rise; 3) End-stage renal disease (ESRD) — about 90% lost, GFR 10-15% of normal, oliguria, oedema

Chronic kidney disease staging (GFR-based)

Stage 1 (damage, normal GFR >90), stage 2 (mild, GFR 60-89), stage 3 (moderate, GFR 30-59), stage 4 (severe, GFR 15-29), stage 5/end-stage (GFR <15)

Haemodialysis vs peritoneal dialysis

Haemodialysis uses an artificial membrane in a haemodialyser, about 6-12 h/week in 3-4 sessions, blood flows past a membrane with dialysate removing wastes and adding glucose/bicarbonate, heparin prevents clotting; peritoneal dialysis uses the patient's own peritoneum, is continuous through daily "exchanges" (3-4 times a day plus overnight) done at home

Renal transplant surgical details

Graft placed in the anterior iliac fossa (space, blood supply, protection, short ureter); donor renal artery/vein anastomosed to the recipient's external iliac artery/vein; ureter joined to the bladder mucosa with the distal ureter wrapped in the muscular bladder wall as a reflux valve; native kidneys usually not removed; only one donor kidney given; lifelong immunosuppressants required

Acute tubular necrosis (ATN)

Damage/death of tubular epithelial cells from ischaemia; the most common cause of delayed graft function and post-transplant AKI; blood flow is normal but tubular function is reduced; surviving cells regenerate over days to 4-6 weeks; typical scan pattern is normal perfusion with reduced/absent tubular function

Transplant rejection types

Hyperacute (within 0-24 h, pre-formed antibodies, poor prognosis, now rare), acute (typically days 5-7 but up to months, T-cell or antibody mediated, reduces perfusion, treated by increasing immunosuppression), chronic (long term, gradual immune-mediated fibrosis, major cause of graft failure)

ATN vs rejection (perfusion is the discriminator)

Acute rejection shows decreased perfusion, delayed transit and excretion, worsens over follow-up; ATN shows normal perfusion, delayed transit and excretion, improves over follow-up

Transplant surgical complications

Urinary leak (failed ureter reimplantation or ischaemic necrosis), urinary obstruction (failed reimplantation, clots, scar tissue, leads to hydronephrosis), vascular occlusion (anastomosis problems, clots, scarring, leads to chronic ischaemia)

Renal Scintigraphy

Functional vs morphological renal agents

Functional agents (filtered or secreted — MAG3, DTPA, EDTA) show perfusion, function, and urine flow; morphological agents (retained in tubules — DMSA) show cortical structure

Tc-99m MAG3

Secreted by proximal tubules via OAT transporters; >90% protein bound (reversibly), so not filtered; peak 3-5 min, 70% excreted by 30 min; measures tubular function and ERPF (effective renal plasma flow); preferred for dynamic imaging, especially in poor renal function

Tc-99m DTPA

Filtered by the glomerulus; <5% protein bound, small molecule; peak ~5 min, 90% excreted by 4 h; measures GFR; extraction fraction only ~20% (poorer than MAG3's ~50%), so a higher dose compensates; less ideal in impaired renal function

Cr-51 EDTA

Filtered by the glomerulus; <0.5% protein bound; 90% excreted by 4 h; measures GFR via blood sampling in a well counter (not imaging — only 9% of decays emit a usable 320 keV gamma, T½ 27.7 days)

Tc-99m DMSA

Retained in proximal tubular cells by binding sulfhydryl groups; slow clearance (~10% excreted at 1 h); maximum uptake at 1-2 h, imaged at 2-3 h (up to 4 h); used for static imaging and SPECT/CT to assess cortical scars, pyelonephritis, and split function; superior to ultrasound for cortical defects

Rule for glomerular filtration vs secretion

A substance must be non-protein bound and small to be filtered; MAG3 fails the non-protein-bound criterion so it's secreted instead; DTPA and EDTA pass both criteria so they're filtered

Tc-99m physical properties for imaging

140 keV, T½ 6 h, pure gamma emitter, ideal for gamma cameras

Renal scan patient preparation

Good hydration before/after injection (poor hydration delays transit and causes cortical retention); void before the scan (a full bladder can mimic reduced function or obstruction); record medications that can disturb renal function (diuretics, ACE inhibitors, ARBs, NSAIDs, chemotherapy) and stop where possible

Standard renography positioning

Supine, arms by side; FOV covers the whole urinary tract (at least half the bladder); H-mode with heads above and below; imaged from the posterior (kidneys lie posteriorly at T12-L3); LEHR collimators, 128x128 matrix, zoom 1

Standard renography protocol phases

Perfusion phase (~2 s/frame x 30 frames, 60 s, showing aorta then renal arteries); uptake/excretion phase (~20 s/frame x 60 frames, 20 min, total 20-30 min, up to 40 min for obstruction/renal failure); pre-void static, then patient walks and voids, then post-void static

Three phases of a renogram

1) Perfusion — blood flow, aorta then renal arteries; 2) Uptake (parenchymal function) — tracer taken up by nephrons (first 1-3 min); 3) Excretion — tracer passes to collecting ducts, calyces, pelvis, ureters, bladder

Renal transit time

How long tracer takes from renal artery entry to the renal pelvis (perfusion plus uptake)

Normal renogram values

Time to peak (Tmax) 3-5 min; T½ peak clearance <10 min; percentage retention (20 min/max) <30% for MAG3; split (differential) function 45-55% measured at 2-3 min; calyces/pelvis fill by ~3 min, ureters/bladder by 5-6 min

Split function calculation

(Counts in one kidney minus background) divided by counts in both kidneys, times 100; measured near peak cortical uptake before activity pools in the collecting system; background counts normalised to the kidney ROI pixel count first

Void imaging purpose

Pre- and post-void images check collecting system patency; walking and emptying the bladder maximises the pressure gradient between pelvis and bladder, letting gravity help drainage; can reveal vesicoureteral reflux

MAG3 vs DTPA clearance

MAG3 clearance reflects tubular secretion, giving ERPF (effective renal plasma flow) with a correction factor; DTPA clearance reflects glomerular filtration, giving GFR adjusted for body surface area, age, and sex; blood sampling is more accurate than camera-based GFR calculation

Obstructive vs non-obstructive hydronephrosis

Obstructive is a physical/mechanical block (stone, tumour, stricture); non-obstructive dilation has no real blockage (e.g. vesicoureteral reflux, functional causes); untreated obstruction can cause obstructive nephropathy

Lasix (diuretic renography) mechanism

A loop diuretic that inhibits the Na+/K+/2Cl- co-transporter, so water follows the ions and urine flow rises; a non-obstructed system washes out tracer, but a fixed narrowed lumen cannot, so tracer is retained

Diuretic renography protocol

Standard baseline renography first; if no retention, stop (no Lasix needed); if retained, patient voids, then ~0.5 mg/kg (20-40 mg) Lasix is given IV slowly, with onset 30-60 s and maximal effect ~15 min

Diuretic renography result interpretation

Normal — half-time <10-15 min after diuretic effect; non-obstructive hydronephrosis — rising curve falls after Lasix (washout); obstructive hydronephrosis — little/no decrease in activity; high-grade obstruction — diuretic has no effect; low-grade obstruction — very slow partial clearance

Captopril renography purpose

Used for suspected renovascular hypertension from renal artery stenosis; captopril is an ACE inhibitor that blocks angiotensin II formation, so in a stenosed kidney the efferent arteriole dilates, GFR falls, and tracer is retained in the cortex

Captopril renography protocol

Stop ACE inhibitors 2-5 days before (would alter baseline), stop diuretics 1-2 days before (risk of hypotension); baseline standard renography done first; then oral captopril (25-50 mg) given, BP monitored until it falls (~60 min), then a second renogram repeated; a positive study is a normal/near-normal baseline with an abnormal post-captopril study in the stenosed kidney

Captopril effect on DTPA vs MAG3 in a stenosed kidney

DTPA shows delayed/decreased uptake (depends on GFR) and increased cortical retention; MAG3 uptake is not hindered (tubular secretion) but shows increased cortical retention because slower filtrate flow delays excretion

Transplant renography technique

Anterior projection centred on the iliac fossa; stretcher mode (heads joined anteriorly) for day-1 patients who are sore/drowsy, H-mode for mobile patients later; bolus must capture iliac artery transit; MAG3 often preferred

Tc-99m DMSA imaging protocol

Inject ~200 MBq IV (no syringe counting needed); image at 2-3 hours to let background clear; supine, arms by side; static anterior and posterior views, ~5 min per view, 256x256; SPECT/CT when possible

DMSA split function calculation

Geometric mean = square root of (anterior counts x posterior counts), calculated per kidney to cancel depth-dependent attenuation; split function = one kidney divided by both kidneys x 100 (normal 45-55%)

DMSA clinical indications

Pyelonephritis, cortical scarring, structural abnormalities, split renal function; often used in children; to assess scarring, scan 3-6 months after the most recent UTI (early-treated pyelonephritis can resolve without scarring)