questions

Question 0

47 year old person with peripheral leg oedema, htn, tachypnoea, urinalysis with red cells, protein, cast and UEC given

1. what features are consistent with acute renal failure
2. How do you calculate GFR
3. how does hyperkalaemia occur? where is potassium stored
4. what complicaiton can occur with high potassium? how does potassium do this?

Answer 0

1. ARK also known as acute renal injury is define as abrupt decline in renal function with increase Creatinine and increase BUN (blood urea nitrogen) over period of several days.

Question 1

Define the following terms:

1. oliguria
2. nephritic syndrome
3. nephrotic syndrome
4. acute renal failure
5. chronic renal failure

Answer 1

1. Oliguria = abnormally low urine output (< 3.5g/day)
   - haematuria
   - azotemia
   - red cell casts
   - oliguira
   - haematuria (glomerula capillary endothelium damage)
2. Nephrotic snydrome (LEAP) = clinical syndrome associated with disorders affecting kidneys, commonly caused by injury to the glomerular basement membrane, define by:
   - Lipid increase
   - edema
   - azotemia
   - proteinuria (> 3.5 g/day)
3. Acute renal failure = rapid decline in renal function occuring over hours/days with increase creatinine and increase BUN (blood urea and nitrogen) which is usually reversible. May have no symptoms, but oliguria is common.

5. Chronic Renal Failure = progressive and irreversible loss of renal function over months/ years, gradual decrease in GFR
GFR values (ml/min): mild 30-50, moderate 10-29, severe /= 90)

Question 2

if 25 year old female presented with anorexia, lethargy, pallor with long history of recurrent urinary tract infections and suffered from several episode of acute pyelonephritis during childhood (none current 5 year), over 12 month noticed increase nocturia. what further aspects of hx and examination are relevant to case?
what investigation?

Answer 2

Time frame of symptoms, if acute (more urgent and potentially reversible)
other symptoms of CRF (MAD HUNGER) from inability to make urine and excrete nitrogenous wastes:
- metabolic acidosis
- dyslipidemia (increase triglyceride)
- hyperkalemia
- uremia (increase BUN and CR, anorexia, N&V, pruritis, malaise, drowsiness, hiccups, seizures, encephalopathy, asterixis, pericarditis, platelet dysfunction - easy brusing), Na/H20 retention (pulmonary oedema - crackles, CHF, hypertension, oedema/ ankle swelling), growth retardation and developmental delay in children, erythropoietin failure (aneamia), renal osteodystorphy (bone pain)

symptoms of ARF - anuria, hypovolaemia, flank pain
childhood enuresis (bedwetting) past 3 yo: associated with vesicoureteric reflux
hx of DM, HTN, vasculitis, drug hx - risk factors)
family of kidney disease (polycystic kidney disease)

Examination:
lung and heart for signs of oedema (na/h20 retention), palpate kidney (palpable may be polycystic kidney disease) and any tenderness

Investigation:
FBC - anaemia
UEC - increase urea, cr, potassium, decrease GFR
24 hour urine collection for protein, nephritic/ nephrotic
MSU if urinary symptoms
Renal U/S - size and cyst
IVP (intravenous pyelogram) - contrast xray via cannula (excrete via kidney) to visualize kidney, ureter, bladder) CI if poor renal funciton and metformin (must stop 24 hrs)
KUB (kidney ureter bladder xray)

Question 3

what are the features visible on IV pyelogram suggestive of kidney damage due to vesico-ureteric reflux?

Answer 3

parachymal scarring of renal cortex (thinning of cortex)
calyceal clubbing (blunting: due to pyelonephritis)
ureteric dilatation

Question 4

what is significance of nocturia, glycosuria? Why do you get increase serum chloride in kidney failure?

Answer 4

nocturia: sign of renal impairment, where kidney cannot concentrate urine normally
glycosuria: renal glycosuria due to impair tubular ability to absorb glucose

increase serum cholride due to hyperchloraemic metabolic acidosis is a normal side effect of HCO3 loss, which is due to decrease resorption of HCO3 in PCT

Question 5

what are the major indication of renal biopsy?

Answer 5

acute nephritic syndrome, unexplained acute/ rapidly progressive renal failure, nephrotic syndrome

Question 6

what is the appearance of kidey in reflux nephropathy cause CRF both macroscopically and microscopically?

Answer 6

macroscopic:
irregular parenchymal scarring with focal thinning of cortex
corticomedullary scarring associated with deformed renal calyx and calyceal clubbing
dilated ureters

microscopic:
tubular hypertrophy/ dilatation
dilated tubules filled with colloid casts
interstitial inflammation and fibrosis of crotex and medulla
inflammatory infiltrate, include neutrophils and macorphages interstitium

Question 7

a 45 year old man complained of progressive lethargy and swelling of ankles over the past 3 weeks. examination revealed a pale and ill-looking man with pitting oedema of both ankles. The JVP was raised 3 cm, there was a fourth heart sound and crepitations were heard at both lung bases. Microscopy of fresh urinary sediment showed granular and red cell casts. over next 24 hours the total urine volume was 400mL.
HR 80, BP 150/110, RR 22, temp 36.3, urinalysis pH 7, protein ++, blood ++, sodium 133, potassium 5.2, cholride 92, bicarbon 18, urea 15, cr 210.
what is your pdx and ddx
what further hx and examination
what investigations

Answer 7

PDX is nephritic syndrome

hx: presenting symptoms, PMHx, Fhx medicaitons
examination: other S and S of uraemia:
- increase BUN and Cr
- N&V, anorexia, pruritis, malaise
- hiccups, drowsy, seizures, encephalopathy
- platelet dysfunction
- asterixis, pericarditis

Question 8

what is the likely pathology of haematuria, oliguria, cast formation in nephritic syndrome?

Answer 8

haematuria: due to immune mediated process -> glomerular inflammation -> increase BM permeability -> RBC escape to bowman’s space -> haematuria
oliguria: immune mediate process -> glomerular inflammation -> glomerular compression, tubular obsturction, arteriolar vasoconstrictio, capillary thrombosis -> decrease GFR -> oliguria

cast formation -> immune mediated process -> glomerula inflammation -> increase BM permeability -> RBC escape into bowman space -> formation of RBC casts from slow tubular flow

Question 9

why in nephritic syndrome, you get HTN, elevated JVP, periphearl oedema?

Answer 9

HTN = immune mediated process -> glomerular inflammation -> glomerula compression, tubular obstruction, arteriolar vasoconstriciton, capillary thrombosis -> decrease GFR -> RAS activation -> HTN

Increase JVP and periphearl oedema = immune mediated process -> glomerular inflammation -> increase BM permeability -> proteins escape into bowman’s space > pronteinuria -> oedema

Question 10

what investigations would you do in nephritic syndrome? how about nephrotic syndrome?

Answer 10

Nephritic:
blood - FBC, U&E, LFT, ESR, CRP, immunoglobulins, electrophoresis, complement (C3, C4), autoantibodies (ANA, ANCA, anti-dsDNA, anti-GBM, blood culture, ASOT, HBsAg, anti-HCV)
urine: rbc cast, MC&S, bence-jones protein
24 urine: protein (protein: creatinine/ albumin:Cr)
CXR
renal U/S
Renal biopsy

nephrotic: same as nephritic + also check cholesterol

Question 11

what is ASOT invesitgations?

Answer 11

asot = anti-streptolysin o titre -> exposure of streptococci, low specification: include culture throat swab and other micro sample like skin swab)

Question 12

Name the different type of nephritic syndrome and which of these are associated with acute renal failure?

Answer 12

acute poststreptococcal glomerulonephritis, rapidly progressive glomerulonephrtiis, diffuse proliferative glomerulonehpritis, IgA nepropathy, Alport syndrome

acute renal failure associated with rapidly progressive glomerulonephritis

Question 13

Describe about acute poststreptococcal glomerulonephritis

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 13

Also known as proliferative GN:
LM - glomerula enlarged and hypercellular (uniform increase -diffuse)
IF - ‘starry sky’, granular appearance (lumpy bumpy) due to IgG, IgM, C3 deposit along GBM and mesangium
EM - subepithelial immune complex (IC) humps - clear over 2 months

most frequently seen in children, occurs 2 weeks after group A streptococcal infection of pharynx or skin cause a type 3 hypersensitivity reaction which resolves spontaneously (95%) - the streptococcal antigen is deposited on the glomerulus cuasing host reaction and immune complex formation

Biopsy is rarely needed if typical of IgG and C3 deposits in IF, serology = incrase ASOT, and decrease C3

renal biopsy will show inflammatory reaction affecting mesangial and endothelial cells

present with peripheral and periorbital edema, dark urine (cola-coloured), HTN, increase anti-DNase B titers and decrease complement
Mx: Renal function will begin to increase spontanesouly within 10-14 days, manage maninly by supportive via adequate fliud, Na restriction, diuretics, hypotensive agent to aim bp less then 130/80 or 125/75 (if proteinuria > 1g/d) - ACEI

pathology due to hypercelluity due to proliferation and swelling of endothelial and mesangial cells by neutrophil and mnocystic infiltrate of kidney

Question 14

describe IgA nephropathy (berger disease)

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 14

IgA nephropathy (Berger disease) is a type of nephritic syndrome, it is the most common GN in developed world, mostly presented with macro/microscopic haematuria.

Typical patient: young male with episodic macroscopic haematuria/ red cell casts, occuring a few days after URTI eg. pharyngitis, recover is rapid between attacks. Can also presents/ flare up with URI/ acute gastroenteritis.

LM - mesangial proliferation
EM - mesangial IC deposits
IF - IgA based IC deposits in mesangium + C3 **
renal biopsy - mesangial proliferation

Mx - general measures. role of immunosuppresion not certain, steroid may decrease proteinuria and slow down decline of renal function, cyclophosphamide in some with rapid deteriorating renal function

Clinical course - last several days, subsites and return every few months, slow progression to CRF in 25-50% in 20 years, worst prognosis if increase BP, male, proteinuira, / renal failure at presentation

ddx of IgA deposite in mesangium = Henoch-Schonlein purpura (IF - IgA based IC deposite in mesangium + C3, properdin, smaller # of IgG and IgM), this is a systemic syndrome invovle skin (pupura rash), GIT (abdo pain), Joint (artheritis), kidney (nephritic)

IgA (main immunoglobulin in mucosal secretion) increase by 50% in patient with this disease

pathology is MAYBE due to increase IgA synthesis in reponse to resp/ GIT exposure to virus, bacteria, food protein -> deposition of IgA and IgA contain immune complex in mesasngium -> activate alternative complement pathway -> glomerular injury

High risk in celiac disease/ liver disease (due to decrease defective hepatobiliary clearance of IgA complex -> secondary IgA nephropathy)

Question 15

Describe about alport syndrome

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 15

Alport syndrome is mutation in type IV collagen -> thinning and splitting of glomerular BM, most commonly x-linked (m > F)

Type IV collagen helps maintain normal function of cochlea, lens and glomerulus, therefore alport syndrome will have glomerulonephritis, deafness (nerve), less commonly eye problems (lens dislocation, posterior cataract, corneal dystrophy)

Question 16

describe about anti-glomerular basement membrane disease

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 16

It is a type of GN (nephritic syndrome), also known as goodpasture’s disease, caused by development of auto-antiboidies to type IV collagen (essential part of GBM). Also found in lungs -> haemoptysis (esp. smokers)

Commonly affect young males, but any age/ gender

Present: macroscopic haematuria + oliguria, renal failure may occur in days of onset

Tx: plasma exchange, corticosteroids +/- cytotoxics (start early can cure and relapse is rare)

Question 17

Describe about diffuse proliferative glomerulonephritis

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 17

Due to SLE/ MPGN, it is the most common death of SLE (1/3 of patients with SLE will have evidence of renal involvement with vascular , glomerular, tubulointerstitial damage)

LM - wire looping of capillaries
EM - subendothelial and sometime intramembrnous IgG based ICs often with C3 deposit
IF - granular

DPGN/ MPGN can present as nephrotic/ nephritic

Question 18

describe about rapidly progressive glomerulonephritis

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 18

it is a type of nephritic*/nephrotic syndrome, GN.
Characterised by rapid + progressive loss of renal function + nephrotic (serve oliguria) and death if untreated

Histology:
Present of cresent* (fibrin + plasma protein) - due to proliferation of parietal epithelial cell of bowman’s capsule + infiltration of monocyte and macrophages
Divided into 3 groups based on immunology, 12% have anti-GBM antibody mediated GN (type I CrGN) +/- lung involvement, 44% have type II CrGN, 44% have pauci immune type III

general:
LM and IF - crescent moon shape ** (cresent consist of fibrin + plasma protein + glomerular parietal cells, monocytes, macrophages)

clinical features = signs of renal failure, features of systemic disease (fever, malaise, myalgia, wt loss, haemoptysis) Massive pulmonary haemorrhage is most common cause of death in those with +ve ANCA

Tx - aggressive immunosuppression with high dose corticosteroids and cyclophosphamide with plasma exchange to remove existing antibodies

Prognosis poor if serum Cr > 600 umol/L, below this 80% improve with tx, present nephrotic like but MORE oliguria & azotemia, proteinuira > 3.5 g/d (maybe), anuric, Long term dialysis/ transplant needed.Prognosis also depend on # of cresent, linear IF)

type II (immune complex mediated 45% of cases)
cause: idiopathic/ postinfectious/ SLE/ IgA neuropathy/ Henoch Schonelein purpura

morphology

• severe injury + segmental necrosis cresent (GBM break), segment without necrosis have underlying immune complex***,
• IF: granular pattern
• EM: deposits

Type III CrGN (50% of cases, 80-90% ANCA +ve)
- causes: idiopathic/ wegener granulomatosis/ microscopic angitis
- wegner = granulomatosis with polyangiitis (PR3-ANCA/ c-ANCA)
- microscopic angiitis (MPO-ANCA/p-ANCA)
= due to lack of anti GBM antibodies/ significant immune complex deposit ion detectable by IF and EM, serum have antineutrophil cytoplasmic antibodies*** (role in some vasculitis), mostly limit to kidney

morphology:

• segmental necrosis + cresent (GBM break)
• uninvolved area is normal
• IF: immunoglobuline and complement -ve, no deposit on EM**

Cresent body formation (shared feature between all RPGN) is from segmental necrosis -> GBM breakdown -> proliferation of parietal epithelial cells + response to exudation of plasma protein (fibrin) into bowman’s space

Question 19

Describe the type of nephrotic syndrome:

Answer 19

focal segmental glomerulosclerosis, membranous nephropahy, minimal change disease, mebranoproliferative glomerulonephritis, diabetic glomerulonephropathy

Question 20

Describe about focal segmental glomerulosclerosis

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 20

= lesion characterised histologically by sclerosis affecting some areas (focal involvement)

account of 20-30% of nephrotic syndrome (idopathic FSG), most common type in african americans, hispanics. important to differtial from minimial change disease in children as MCD response well to steroid thearpy while FSG have poor response to steroid thearpy 30% only and may -> CRF (FSG have higher HTN and hematuria)

Cause: idiopathic/ HIV infection, sickle cell disease, herion abuse, massive obesity, interferon tx, chronic kidney disease due to congenital absence/ surgical remove

Pathogensis:
unknown, suggestion are MCD -> FSG, injury to podocyte, permeability increase factors produced by lymphocyte (like MCD), deposit of hyaline masses in glomeruli represent entrapment of plasma protein and lipid in foci of injury where sclerosis develop and IgM and complement, circulating mediator cause damage to podocyte (24 hr of transplant -> recurrence of FSG)

LM - segemental sclerosis and hyalinosis
IF - neg, IgM and C3 deposit affected
EM - effacement of foot process similar to minimal change disease
morphology: segmental and focal involvement, increase mesangial matrix, obliterated cap lumen, deposit of hyaline masses (hyalinosis) and lipid droplet
progression of disease -> global sclerosis of glomeruli with pronounced tubular atrophy and interstitial fibrosis

Question 21

Describe minimal change GN

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 21

Most common type of nephrotic syndrome in children (76%) and 20% adults, it is benign with no HTN and renal function preserve with selective proteinuria (commonly albumin).

May be triggered by recent infection, immunization, immune lymphoma (eg. cytokine-mediated damage)

Tx: steroid + cyclophosphamide/ cholrambucil if renal function deteriorates; excellent reponse to corticosteroids (>90% response but 2/3 may remit -> steroid dependent)
- adults also response to steroid but slower and more relapses

Prognosis:
good prognosis with CRF in 25 years, 40% have spontaneous remission,

LM - normal glomeruli (lipid in PCT cells + protein deposit)
EM - effacement of foot process (uniforma nd diffuse)
IF - neg

Question 22

Describe membranous nephropathy

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 22

Causes:
MOST COMMON cause of primary nephrotic syndrome in caucasian adults
- 85% idiopathic
- 15% other: infections (chronic hep b, syphilis, schistosomiasis - disease caused by parastici worm infect urinary tract/ intestin), malignant tumour (ca of lung, colon, melanoma), SLE/ other autoimmune, exposure to inorganic salts (gold, mecury), drug (peniclinamine, captopril, NSAIDs)

pathology: unknown, induced by antibodies reacting in situ to endogenous/ planted glomerular antigens; type of chronic immune complex nephritis

morphology:
LM - diffuse capillary and GBM thickening (may be normal early on)
IF - granular as result of immune complex deposit (IgG and C3 subepithelial deposit)**
EM - “spike and dome” appearance with subeptiehlial deposits
- spike and dome = part by subepithelial deposits that nestel against GBM seperated by small spikelike protrusion of GBM matrix form as disease progress, spike close over deposit -> incoporatedin GBM and podocyte show effacement of foot process -> catabolized -> dissappear -> cavities in GBM + continue deposit in BM matrix -> progressive thicker BM -> sclerosed of glomeruli

Clinical course:
slow progressive, common in 30-50years old, 40% will spontaneous remission
poor response to steroid, 60% proteinuria persist, 4-% may -> CRF in 2-20years, 10-30% have benign course with partial/ complete remission of proteinuria
steroid + cyclophosphamide/ chlorambucil if renal function decrease (poor prognositc factors are decrease renal funciton, heavy proteinuria)

Question 23

describe amylodosis nephrotic syndrome

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 23

LM - congo red stain show apple-green birefringence under polarized light
kidney most commonly involved organ in systemic amylodosi, associated with chronic conditions (eg. multiple myeloma, TB, RA)

Question 24

describe diabetic glomerulonephropathy

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 24

LM - mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesion)

Nonenzymatic glocosylation of GBM -> increase permability, thickening

nonenzymatic gloycosylation of efferent arterioles -> increase GFR -> mesangial expansion

Question 25

describe membranoproliferative glomerulonephritis

what it is, LM, IF, EM, epidimiology, pathology, morphology, tx and clinical prognosis

Answer 25

= alteration of GBM, mesangium, proliferation of glomerular cells
represent 5-10% of idiopathic nephrotic syndrome, some present with hematuria/ proteinuira in non-nephrotic range, some with nephritic + nephrotic

Type I (more common, 80%)

• subendothelial immune complex deposit with granular IF; tram track (glomerular capillary wall double countour (esp in PAS stain - periodiacid schiff stain) appearance due to GBM spiltting caused by mesangial growth
• decrease C4 (classical complement) + IgG
• associated with HBV, HCV, idiopathic,

type II

• intramembrouns IC deposit, dense deposit
• decrease serum C3, and C3 nephritic factor (alternate complement activation)
• associated with C3 nephritic factor (stabilizes C3 convertase -> decrease serum C3 levels)

LM: both
glomerular large with accentuated lobular appearance + proliferation of mesangial and endothelial cell + infiltrate leukocyte

Tx: none proven, prognosis 50% -> ESRF and can recur after transplant

Question 26

pathology of nephrotic syndrome, why they get LEAP? also what is the difference between disease that occur in children and adults?

Answer 26

1. dearangment in capillary wall of glomeruli -> increase permeability to plasma protein (increase permeability due to structural/ physiochemical alterations allow protein to escape from plasma into glomerular filtrate; endothelium, GBM, podocyte are barrier)
2. long standing/ extreme heavy proteinuria, serum albumin decrease -> hypoalbuminemia (decrease in plasma colloid osmotic pressure) + primary retention of Na and H20 (kidney) -> proteinuira
3. then fluid escape from vascular tree -> tissues -> decrease plasma vol. + decrease GFR, therefore aldosterone secretion + decrease GFR + decrease secretion of Nat riuretic peptide -> Na and H2o retention -> more edema -> anasarca (general edema)
4. Children (1 to 7 years old) lesion primary to kidney, adults commonly due to systemic disease (eg. DM, amylodosis, SLE)

Question 27

describe hypoalbuminemia in nephrotic syndrome

Answer 27

hyperlipidemia -> hypoalbuminemia -> increase synthesis of lipoprotein in liver + abnormal transport of circulating lipid particle impair peripheral breakdown of lipoprotein (GBM increase permeability to lipoprotein

Question 28

in nephrotic syndrome, patient was found to have 6.5 grams of protein in 24 hours, describe how does protein reach urine and what are main type of protein present?

Answer 28

due to derangement in capillary wall of glomeruli -> increase permeability to plasma protein, increase filtration of macromolecules to cross glomerular capillary wall

Protein mainly found is albumin on dipstick

Question 29

what clinical problems can occur as a result of heavy proteinuira>

Answer 29

renal disease -> renal failure

HTN: increase risk of further renal disease, MI, Stroke

Question 30

what is haematuria? if +ve dipstick is that enough to dx?

Answer 30

frank haematuria = blood/clot in urine noticed by patient
microscopic haematuria = blood by dipstick/ sediment

+ve dipstick require confirmation by urine microscope due to high false +ve results

Question 31

what are some causes of haematuria?

Answer 31

fairly common:

• calculus (also affect ureters)
• infection

less common:

• glomerulonephritis
• renal cell carcinoma/ nephroblastoma
• transitional cell carcinoma

uncommon:

• hyphronephrosis due to pelvic ureteric junction obsturction
• polycystic kidney
• papillary necrosis

rare:
- bleed diatheses (anticoagulant)
bacterial endocarditis -> embolism in kidney
AF -> embolism in kidney

other differiation:
exercise haemaglobinuria + haematuria - young after vigourous exercise
women of bearing age may have due to manstruation

Question 32

how do you differiate blood from kidney/ ureter/ bladder?

Answer 32

blood from kidney,ureters/ bladder wall will completely mix with urine and present throughout stream

urethral bleed may leak out idenpentaly/ beginning on end of urine stream

blood from bladder neck/ posterior urethra may present as terminal haematuria

Question 33

describe method for detection of blood in urine, describe ways of appearance of red cells may differ in relation to origin of bleed?

Answer 33

method:

• dipstick (macroscopical red colour/ smoky urine)
• microscopy (> 2-3 rbc/ hpf in centrifuged sediment of 10-12mL urine)

appearance of RBC

• cast: made in tubule but source of bleed glomerular/ tubule
• amorphic (squished) = glomerulus
• isomorphic (normal) = post-glomerular

Question 34

list cause of haematuria in terms of pre-renal, renal, post-renal cause

Answer 34

pre-renal:

• anticoagulation
• coagulopathy (haemophilia, thrombocytopaenia)
• other haematological disorders

renal:
infection, tumour, trauma, acute tubular necrosis, calculi, glomerulonephritis, vascular, surgery, cysts, drugs (eg. gentamycin, cisplatin, rifampicin, sulphonamides, contrast agenst, cyclosporin, chemotherapeutic drugs)

post renal (calyes downward)
- trauma (in dwelling catheter, foreign body, rapid empty)
tumour (transitional cell carcinoma)
infection (cystitis, urethritis, prostatisit)
calculi
surgery
drugs (cyclophosphamide), chemical (phenols, turpentine)

commonest cause by age and sex

0-20 year old - UTI, acute glomerulonephritis, congenital (eg. cystic kidney/ horseshoe kidney)

20-40 years old: UTI, genital trauma, calculi, TCC

40-60: UTI, TCC, calculi

> 60 year old:

female: UTI, TCC, vaginal trauma, calculi
male: UTI, benign prostatic hyperplasia, TCC, calculi, trauma

Question 35

what does red blood cast mean and describe it, what common cause of red blood cast?

Answer 35

rbc sticks together and form casts, yellow borwn, cylindrical with sometimes ragged edges, fragile, indicates gloermular damage (glomerunehpritis/ vasculitis), severe tubular damage, associated with renal infarction and subacute bacterial endocarditis

Question 36

what is the investigation of patient with persistent haematuria?

Answer 36

MSU - MCS
1. Culture -ve
a. Cr CT/ IVP (stones, tumour, anatomical anomaly)
b. Cr > 120 umol/ L -> U/S (size, shape, position, enlarged/ cystic, stricture, +/- stones)
if normal ->
young ( renal biopsy
old (> 45), lower urinary tract symptoms -> urine cytology, cystoscopy
2. Culture +ve - treat

urinalysis

• dipstick blood +ve but no RBC microscopally = haemoglobinuria/ myoglobinuria
• proteinuria > 0.5 g/24 hr/ red cell case/ spiculated rbc = glomerular disease
• isolated: calculi/ neoplasm

cytology: screen for TCC
urinary calcium and urine acid in 24 hr sample: calculi
plan abdominal xray: calculi
abdominal U/S: simple cysts, ureteric dilation
IVP: outflow obstruction
CT, MRI”: renal and bladder tumour
cystoscopy/ retrograde pyelography: lesion involve bladder, ureter, renal pelvis
angiography”: renal tumours
FNA and open biopsy

Question 37

describe the four different types of kidney stones and predisposing factor for developing stones?

Answer 37

Kidney stones can lead to severe complications (hydronephrosis, pyelonephritis), present with unilateral flank tenderness, colicky pain radiate to groin, hematuria. Treat and prevent by fluid intake.

Predisposing factors:

• supersaturated urine i.e excess Ca, PO4, urate
• stasis, change in urine pH (renal disease, recurrent infection)
• lack of urinary inhibitors of crystallization (citrate, pyrophosphate)

Types:
1. Calcium (80%)
precipitates at increase pH (calcium phosphate)/ decrease pH (calcium oxalate), xray (radiopaque), crystal (envelop/ dumbell shape)
promoted by hypercalciuira (idiopathics/ 2 degree to hypercalcemia like cancer/ increase PTH)
calcium oxalate can be due to ethylene glycol (antifreeze), vitamin C abuse, crohn disease
tx for recurrent stone = thaizide and citrate
MOST COMMON STONE = calcium oxalate stone with hypercalciuria and normocalcemia

ammonium, magnesium, phosphate stone (struvite stones) (15%)
- precipitates at increase pH, radiopaque, crystal is like coffin lid
Cause by infection with urease positive bug (eg. proteus mirabilis, staphylococcus, klebsiella) that hydrolyze urea to ammonia -> urine alkalinization
can form staghorn calculi -> nidus for UTI
tx: eradicaiton of underlying infection and surgical remove of stones

Uric acid (5%)
- precipates at decrease pH, radioLUCENT, crystal like rhomboid/ rosettes shape
risk factors: decrease urine volume, arid climates, acidic pH
visible on CT and U/S, NOT XRAY
strongly associated with hyperuricemia (eg. gout), seen in disease with increase cell turnover like leukemia
tx alkalinization of urine

cystine stones (1%)
precipitants at decrease pH, radiopaque, crsytal shape like hexagonal
mostly seen in children, second degree to cystinuria, can forn staghorn calculi, sodium nitroprusside test +ve
tx: alkalinizaiton of urine and hydration

Question 38

how patient who chronically ingested compound analgesic can cause haematuria?

Answer 38

analgesics like aspirine and phenacetin can cause by tubulointerstitial nephritis -> atrophy -> fibrosis -> renal failure

phenacetin metabolites directly toxic to tubules

aspirin reduce blood flow to medulla and papillae cause ischaemic injury by local prostaglandin inhibition

Question 39

describe cause and pathophysiology of renal colic

Answer 39

smooth muscle peristalsis against obsturcted ureter, starts at flank radiate anterioly to abdomen and ipsilateraly to testis/ labium, tender on palpiation associated with N&V
cause: caluli (stones), blood clots, necrotic papillae, tumour fragments