Kidney, Urinary Tract and Electrolytes Flashcards
subendothelial immune complex deposition is which pathology?
type I membranoproliferative glomerulonephritis
what is bethanechol?
mAChR agonist used for acute neurogenic urinary retention
pathophysiology of acute interstitial nephritis?
drug-induced hypersensitivity reaction involving the interstitium and tubules in the kidney, leads to AKI
what molecules do you use to estimate GFR and RPF?
GFR = inulin, freely filtered and neither secreted nor resorbed
RPF = para-aminohippuric acid (PAH), combination of filtration and secretion means that all PAH entering the kidney is lost to the urine
which disease predisposes to angiomyolipoma? what is this tumour?
tuberous sclerosis hamartoma of connective tissue
2 classes of aetiology for acute tubular necrosis?
- nephrotoxic
- ischaemic –> consequence of prerenal AKI
non-enzymatic glycosylation occurs preferentially at which site of the glomerulus in DM?
efferent arteriole leads to hyaline arteriolosclerosis, increased pressure in the glomerulus leading to hyperfiltration
Minimal change disease histological findings? Immune fluorescence?
nil on light microscopy effacement of the podocyte foot processes on EM nil on IF
what are the two main embryonic structues giving rise to kidey and what do they turn out to become?
- ureteric bud - ureters, calyx, pelvis, collecting ducts
- metanephric mesenchyme - glomerulus through DCT
which diuretics lead to low urine Ca++
thiazides
pathoG - muddy brown casts
acute tubular necrosis
6 aetiologies of nephrotic sydnrome
- minimal change disease 2. focal segmental glomerulonephritis 3. membranous nephropathy 4. MPGN 5. diabetes mellitus 6. systemic amyloidosis
what is the effect of ACE-I on glomerular filtration rate?
inhibit ACE, decrease AT II, prevent constriction of efferent arteriole
decreases GFR
location of immune complex in membranoproliferative glomerulonephritis type 2 - ‘dense deposit disease’
associated condition
intramembranous
positive C3 nephritic factor (autoantibody), constituent conversion of C3, leading to nephritic syndrome
(lab finding = decreased circulating C3)
a shrunken, cystic kidney suggests what pathology?
end-stage renal failure on dialysis
association with horseshoe kidneys (2)
ureteropelvic junction obstruction and hydronephrosis
stones and infection
focal segmental glomerular sclerosis disease association(s)
HIV, sickle cell disease, heroin abuse
what is this?
underlying condition?
renal angiomyolipoma
associated with tuberous sclerosis
nephrolithiasis shape = coffin lid, rectangular prism radio opaque
Magnesium ammonium phosphate (MAP)
site of action of mannitol?
where the tubule is permeable to water freely
PCT and dLH
in a woman, ureter passes infront of what artery and underneath what artery in the pelvis?
infront - internal iliac
behind - uterine (within uterosacral ligament)
focal segmental glomerular sclerosis race association
Hispanic and African-American
Churg-Strauss features (4)
- RPGN 2. asthma 3. eosinophilia 4. granulomatous inflammation
nephrolithiasis shape = diamond or rhombus non radio opaque
urate
a heroin addict presents with nephrotic syndrome - what is the most likely pathology?
focal segmental glomerulonephritis
crystalisation of urate crystals occurs where in the nephron? why?
collecting ducts low pH
blood supply to the proximal ureters
blood supply to the distal ureteres
renal arteries
superior vesical arteries
spike and dome appearance on IF is suggestive of what pathology?
membranous nephropathy
patient with SLE develops nephritic syndrome. what is the most likely pathology?
diffuse proliferative glomerulonephritis which is one of the Rapidly Progressive Glomerulonephritides
RPGN IF findings = granular (2)
Immune complex mediated PSGN or diffuse proliferative glomerulonephritis
equation for filtration fraction?
FF = GFR/RPF
major complication of PSGN?
rapidly progressive glomerulonephritis - renal failure in weeks to months
metolazone is what?
thiazide diuretic
what is the normal handling of potassium along the nephron?
free filtration at the glomerulus, 70% isotonic resporption at PCT
20-25% resorption across NKCC in TALH
point of control = DCT and collecting duct
excretion through principal cells (Na/K ATPase), resorption in alpha-intercalated cells
increase excretion = high extracellular K+, aldosterone, alkalosis
nephrolithiasis shape = hexagon radio opaque
cystine
3 diseases associated with Wilms tumour
- WAGR 2. Denys-Drash syndrome 3. Beckwith-Wiedemann syndrome
5 nephrotoxins that can cause acute tubular necrosis?
uric acid - tumour lysis syndrome
aminoglycosides
ethylene glycol (associated oxalate crystals in urine)
heavy metals - lead
myoglobin (crush injury)
what are the nephrotoxic effects of amphotericin B?
decreased GFR and direct toxicity to the epithelium
results in anaemia (decreased EPO), hypokalaemia/hypoMg++
asymptomatic with one hypertrophied kidney at birth?
congential solitary functioning kidney
EPO is produced by which cells?
renal peritubular interstitial cells
what is normal GFR?
125 mL/min
2 clinical features of renal papillary necrosis?
gross haematuria and flank pain
what is the final structure of the developing kidney to canalize?
uteropelvic junction - detected on USS as hydronephrosis
most common site of obstruction
what is the benefit of ARB over ACE-I?
does not give bradykinin symptoms
functional definition of nephrotic syndrome
> 3.5 g/day protein in 24 hour urine collection
4 causes of renal papillary necrosis
- analgesic abuse (aspirin or pheacetin) 2. diabetes mellitus 3. sickle cell disease (or trait) 4. severe, acute pyelonephritis
isolated haematuria & hearing loss suggest?
Alport syndrome (also ocular disturbance and X-linked inheritance pattern)
which diuretics lead to acidaemia?
- carbonic anhydrase inhibitors (acteazolamide)
- potassium sparing diuretics
reduced secretion of K+/H+ in DCT/CD; hyperkalaemia forces protons out of cells through K+/H+ antiporter
which diuretics cause an increase in urine potassium?
mostly loop and thiazide diuretics, hence hypoK+
what is the site of action of acetazolamine in the nephron?
PCT and dLH
which diuretics lead to alkalosis and what are the 3 mechanisms?
loop diuretics and thiazides
- contraction alkalosis - total volume decrease, RAAS activation, Na+/H+ resorption in PCT, HCO3- follows, total body bicarb increases
- loss of K+, hypokalaemia pulls K+ out of cells forcing H+ into cells out of plasma
- paradoxical aciduria - hypokalaemia means H+ rather then K+ is secreted for Na+ resorption in DCT/CD across Na+/K+ transporter
RPGN IF findings = linear (1)
Goodpasture IgA bound in a line to GBM
prenatal hydronephrosis and thickened bladder wall suggests…?
posterior urethral valve
only in males, most common bladder outlet obstruction
patient with SLE develops nephrotic syndrome. what is the most likely pathology?
membranous nephropathy
4 blood findings with nephrotic syndrome
- hypoalbuminaemia 2. hypogammaglobulinaemia 3. hypercholesterolaemia 4. hypercoagulability - selective loss of antithrombin III
subepithelial immune complex deposition is which pathology?
membranous nephropathy
renal blood flow = 1.0
GFR = 0.1
haematocrit = 0.5
what is the filtration fraction?
FF = GFR/RPF; RPF = RBF * (1 - Hct)
FF = (0.1) / (1.0 - 0.5) = 0.2
bugs causing cystitis
E Coli (80%) Staph saprophyticus (young, sexually active women) Klebs pneumoniae Proteus - alkaline urine Enterococcus faecalis
what is the site and mechanism of action of potassium sparing diuretics?
DCT and collecting duct
Na+ channel blockers/reduce expression
where is the site of PTH action in the nephron? what channel and what is the net result?
proximal CT
inhibits NaPi cotransport, increasing PO43- excretion
distal CT
stimulates Na+/Ca++ exchange at the basolateral surface, increasing Ca++ resorption
how long following an episode of acute tubular necrosis does normal kidney function return?
3 weeks
location of immune complex in membranoproliferative glomerulonephritis type 1
associated condition
subendothelial
Hepatitis B & C
what’s the formula for clearance of substance in the kidney?
clearance of ‘x’ = [x]urine * (urine flow)/[x]plasma
urine flow usually in mL/min, just make sure units for concentration are equivalent
pathoG Kimmelstiel-Wilson
Diabetes mellitus sclerotic nodules formed in the glomerular mesangium
what are the adverse effects of potassium sparing diuretics?
hyperkalaemia
spironolactone = anti-androgen effects (gynaecomastia)
where does horseshoe kidney get stuck?
inferior mesenteric artery
pathoG - eosinophil in urine
acute interstitial nephritis
caudal end of mesonephric duct (mesoderm) produces what structure?
bladder trigone
where the rest of the bladder is endoderm
what are the metabolic effects of loop diuretics?
- hypokalaemia
- contraction alkalosis (activation of RAAS following contraction dumps H+ in exchange for Na+)
which kidney do you take in transplant donation and why?
left kidney b/c longer renal vein
membranous nephropathy is associated with which 4 conditions?
SLE HBV HCV solid tumours
what does mesonephros do?
interim kidney for 1st trimester then degenerates
forms part of male genital system
focal segmental glomerular sclerosis histological findings? EM/Immune fluorescence?
sclerosis (collagen deposition) of only a segment of the glomerulus (H&E)
effacement of the podocyte foot processes on EM
nil on IF
complications of duplex collecting system
viscoureteric reflux and ureteral obstruction (UTIs)
pathoG - white blood cell cast
pyelonephritis
RPGN IF findings = negative (3)
Wegener’s granulomatosis (cANCA) microscopic polyangiitis (pANCA) Churg-Strauss syndrome (pANCA)
tumour lysis syndrome prophylaxis
- adequate hydration (good GFR, less likely to build up toxins in tubule) 2. allopurinol - limit the conversion of amino acids to uric acid all in one go
the classic triad of RCC
haematuria palpable mass flank pain
what is the most common cause of nephrotic syndrome in otherwise healthy Caucasian adults?
membranous nephropathy
immune signalling mechanism leading to glomerular inflammation in nephritic syndrome
- immune complex deposition
- activation of complement C5a
- activation attracts neutrophils (hypercellular on H&E)
- neutrophils mediate inflammation and damage
a large, cystic kidney suggests what pathology?
polycystic kidney disease
what is the mechanism of acyclovir nephrotoxicity?
renal excretion
if concentration builds up in collecting duct then crystalisation and renal tubular damage will occur
prophylaxis with aggressive IV fluids
what is the site and mechanism of action for thiazide diuretics?
inhibit NaCl reabsorption in DCT
reduces Ca+ excretion
pathoG waxy casts
chronic pyelonephritis, chronic kidney disease, end-stage renal failure
what are the adverse effects of foscarnet and what are the mechanisms?
hypocalaemia and hypomagnesaemia
- direct chelator of calcium
- renal wasting of magnesium, decrease PTH, exacerbate hypoCa++
nephrolithiasis shape = octahedron radio opaque
calcium oxalate
pathoG subepithelial hump
post streptococcal glomerulonephritis
what are the adverse effects of loop diuretics?
think: direct effect, metabolic disturbance, hypersensitivity
ototoxicity
hypoK+/Mg++, metabolic alkalosis
sulfa allergy/interstitial nephritis
which drug therapy is best management to prevent development of renal failure in a diabetic?
ACE inhibitor
what is the effect of the sympathetic nervous system on RAAS?
sympathetic action on beta1-adrenoceptors on macula densa increases renin secretion
beta-blockers main action on hypertension is through decreasing RAAS
failure of the ureteric bud to induce proper differentiation of the metanephric mesenchyme results in what disease?
multicystic dysplastic kidney
gold standard for UTI diagnosis
>100,000 colony forming units on urine culture
what embryonic tissue gives rise to the kidneys?
metanephros
brown, granular casts in the urine suggests what pathology?
acute tubular necrosis necrotic cells plug the tubule, casting into shape and obstructing flow, decreasing GFR. eventually pass through into the urine
chlorthialidone is what?
thiazide diuretic
when does pronephros degenerate?
by week 4
what is the site and mechanism of action of loop diuretics?
2 examples
thick ascending LH
inhibit NKCC cotransport, natriuresis.
increase excretion of Ca++ ‘loops lose Ca++’
furosemide, bumetanide, torsemide, ethacrynic acid (nonsulfa drug)
presence of ‘M protein’ refers to which organism? what is the clinical relevance?
group A beta-haemolytic streptococcus increases the chance of developing PSGN following skin or pharynx infection
what are the benefits and risks of using ethacrynic acid over furosemide?
cannot induce sulpha allergy
more ototoxic
pathoG red cell cast
nephritic syndrome glomerular bleeding
what are the histopathologic findings in membranous nephropathy?
light microscopy = thickened GBM EM = subepithelial immune complex deposit with ‘spike & dome’ appearance IF = granular deposits
biopsy - uniform, diffuse thickening of the basement membrane without an increase in cellularity suggests which pathology?
membranous glomerulopathy
what are the adverse effects of thiazide diuretics?
hypoK+/Na+ metabolic alkalosis
hyperGLUC -glycaemia, lipidaemia, uraemia, calcaemia
triamterene is what?
Na+ channel blocker in cortical collecting duct, K+-sparing diuretic
same action as amiloride
acetazolamide causes alkalosis or acidosis?
reduces resorbtion of bicarb, so you lose total body HCO3-
Resulting in acidosis
decreased kidney perfusion causing pre-renal AKI affects which portion(s) of the nephron first?
proximal convoluted tubule and thick ascending limb of loop of henlé - both in renal medulla which has poor oxygen supply even in physiological conditions
glomerular sclerosis and hyalinosis would suggest which pathology?
diabetic nephropathy
intramembranous immune complex deposition is which pathology?
type II membranoproliferative glomerulonephritis
eplerenone is what?
aldosterone antagonist, K+-sparing diuretic
nonfunctional kidney consisting of cysts and connective tissue..
diagnosis?
mutlicystic dysplastic kidney
which diuretics lead to loss of Ca++
loop diuretics
renin is released by which cells in the kidney?
juxtaglomerular cells which are modified smooth muscle cells located around the wall of the afferent arteriole
