Nephro SAQ Flashcards
30 year old man, presents with an incidental finding of microscopic haematuria during a health check up after purchasing a health insurance plan. He has been completely asymptomatic all along, with no changes in his urinary habits / colour. APPARENTLY (this wording is so weird), he has a cousin who was diagnosed with a chronic kidney disease at aged 20. On physical examination, his blood pressure was 120/88 mmHg, the examination was otherwise unremarkable. His lab results are as follows:
RFT: slightly raised creatinine, normal albumin
Urine: 15 red blood cells on microscopy (didn’t specific high power field), protein 1+
- Name ONE most relevant imaging modality (2) and name TWO findings that you would look for (4).
- What further urine test would you do to guide your diagnosis / management? (2)
- What is a likely underlying parenchymal disease? (2)
- USG (loss of corticomedullary differentiation, small kidneys)
- 24 hour urine albumin quantification (determine how severe protein loss)
- IgAN, PKD
66/M hiking and falls, unconscious and rescued 2 days later.
Blood tests:
Sodium normal
Potassium 7.1
Urea elevated 300
Creatinine ~1000
Patient passed very little urine in the past 4 hours
Nurse noticed it was red in colour
Urine dipstick showed 2+ protein and 3+ RBC
- Urine test most helpful for diagnosis (1)
- Investigations to help diagnose or manage his condition (4)
- Most likely RENAL diagnosis (1)
- What is the Immediate Management (2)
- Urine +ve for myoglobin, red or brown +ve for blood but no RBC under microscopy, pigmented granular casts in the urine
- CK level, electrolytes levels (hypoCa, hyperP, hyperuricemia), ABG (metabolic acidosis), DIC
- ATN due to rhabdomyolysis
- Calcium gluconate + sodium bicarbonate + insulin/dextrose drip +/- Haemodialysis (if not responsive). treat the rhabdo with forced diuresis (IV fluids)
70s/F, presenting with nasal bleed (further assessment confirmed sinusitis or smth), 5kg weight loss for 3 months. Fever.
CXR shows diffuse patchy infiltrates
a) Markedly elevated creatinine, high urea.
Based on the kidney function, suggest urine investigations (2)
b) Based on the CXR findings, what non-invasive investigations would you perform? (2)
c) Suggest 1 serological test (2)
d) What is your diagnosis?
e) Name 2 management options (2)
a) urine microscopy (confirm haematuria with dysmorphic red cells and cellular crescents
b) bronchoscopy
c) ANCA (p-ANCA pattern (MPO-ANCA: GPA and MPA) and c-ANCA (PR3-ANCA: EGPA) represents the immunofluorescence staining pattern)
d) GPA
e) steroid, immunosuppressants, IVIG, rituximab
Old woman flu-like symptoms, self-bought medicinal oil over the counter 1w ago. Now confused and tachypnoea. Uncooperative to PE. Normal CNS (able to move 4 limbs, no focal neurological deficit and neck stiffness) and RS (clear chest) PE.
Blood gas:
Sodium 136, potassium 6, chloride 102, bicarbonate 8
Urea 12.7, Creatinine 212
pH 7.26
- Describe the acid-base disorder in the blood gas.
- Name 4 investigation to determine the cause.
- 2 immediate measure to lower plasma K.
- If the blood gas shows marked respiratory compensation and hyperventilation, what is the most likely cause?
- High anion gap metabolic acidosis (pH < 7.26 so metabolic acidosis), (136- (102 +8)) = 26 (above normal anion gap)
- Serum salicylate level, urine toxicology, lactate level, blood glucose and ketones
- IV 10% calcium gluconate, IV regular human insulin, K, resonium C, nebulized salbutamol
- Salicylate poisoning
A young lady with known MVP was diagnosed with infective endocarditis. Blood culture showed streptococcus viridians and she was placed on ampicillin and gentamicin. 2 weeks later, she developed shortness of breath and ankle swelling. She developed erythematous macular rash over on trunk and LL. Creatinine level was raised. Urinalysis showed positive RBC 1+ and protein 1+.
1. Name 3 possible differentials
2. Name 4 non-invasive investigations for confirmation of diagnosis
3. Name 3 indications that would require temporary dialysis for this patient
- Acute interstitial nephritis due to ampicillin
Post infective endocarditis glomerulonephritis
Septic emboli from IE to renal artery
Acute tubular necrosis (TIN) due to gentamicin (aminoglycoside)
DRESS causing AKI - Urine for WBC cast, eosinophilia, RBC cast for AIN and GN
CBC for eosinophilia
C3/4 for glomerulonephritis
Renal artery ultrasound for septic emboli
Serum gentamicin level (trough level) - Refractory hyperK >6, refractory metabolic acidosis <pH<7.1) but c/i to HCO3, refractory pulmonary edema, uremic pericarditis/encephalopathy
F/35 with CKD due to IgA nephropathy. Husband with good past health wants to donate his kidney.
1. 2 prerequisites
2. Like recipient and donor 3, how many HLA mismatches?
3. Patient given steroid, cyclosporin and MMF after transplant. MoA of cyclosporin
4. 2 AE of MMF
5. Patient developed elevated creatinine on post-transplant day 12. (Table showed Cr level and cyclosporin trough up level from day 1 to 12, Day 12 trough pending) 3 reasons for elevated creatinine on day 12
- No CJD, degenerative neurological disease. No history of IVDU. No HIV+ve. No malignant disease (except primary BCC, carcinoma in situ of uterine cervix), known cause of death
- 0 mismatch
- Inhibit calcineurin, inhibit IL2 synthesis
- GI upset, VZV infection, teratogenicity, myelosuppression. CMV infection, hypertension
- Infection: bacterial, viral (BK, JC virus)
* Urine outflow obstruction
* Acute rejection
* Impaired arterial supply (transplant artery stenosis)
* Calcineurin inhibitor nephrotoxicity (hence measure trough level)
* Nephrotoxicity from other medications e.g. NSAIDs, TCM
* Renal vein thrombosis
a)
Hypovolemia (prerenal cause) due to diarrhea
Calcineurin inhibitor nephrotoxicity
Antibiotics tubulointerstitial nephritis
NSAID induced nephrotoxicity
b) Optomize preload for hypovolemia: normal saline 500-1000ml over 1-2 hours
c)
d) Hypovolemic hypernatremia due to excessive renal loss of water
e) Volume repletion 1/2 NS or NS than correct tonicity: PO or IV hypotonic fluids
a) Iron profile (early iron deficiency anemia)
b) Reticulocyte cunt, ferritin/Tf saturation and serum B12/folate to exclude non renal causes of anemia
c)
Hb<10: start on erythropoiesis stimulating agents e.g. mircera
Iron supplementation to be given before ESA when iron deficient. Choice: oral FeSO4, IV Fe sucrose
dietary retriction of phosphate containing food. Calcium containing phosphate binders: calcium acetate
A 30+ year old man presents with significant oedema of the lower limbs after a URTI. The following laboratory results are obtained (urine ++ protein).
a. What is the clinical diagnosis?
b. List 3 complications of this condition
He is given furosemide by his GP but his condition doesn’t improve.
c. What is the problem with the medication given by the GP
d. What serological markers can be used to aid diagnosing the problem?
e. What is the likely histological diagnosis
f. What treatment is usually given for this diagnosis?
a. nephrotic syndrome
b. AKI, hypovolemia, increased risk of infection (loss of Ig), increased thrombotic risk, hyperlipidemia (to compensate for loss of albumin)
c. Removes fluid but does not relieve the oncotic pressure difference
d.
Minimal change disease
FSGS: anti GBM
Membranous nephropathy: primary (anti PLA2R), secondary. Infection: HBV, HCV, HIV, malaria, syphilis. Drugs: NSAIDs. Class 5 lupus nephritis: serum C3/4, ANA, anti dsDNA
e. Minimal change disease
f. Plasmapharesis (wash out the anti GBM antibdoies) + Oral prednisone (1mg/kg) + oral cyclophosphamide (2-3/mg/kg/day)
A 76-year-old Chinese female housewife presents with severe ankle swelling for one week. She has a history of hypertension for 10 years and has been taking amlodipine 5 mg daily for 8 years with blood pressure readings of approximately 120/80 mmHg, and has been asymptomatic all along. Physical ex- amination shows bilateral severe pitting ankle oedema, blood pressure of 122/78 mmHg, and normal findings otherwise. Urine test strip (dipstick) shows 4+ proteinuria, and microscopy shows no red blood cells or white blood cells. Investigation results are as follows: serum creatinine 76 umol/L (normal 82– 126 umol/L), serum albumin 18 g/L (normal 38–46 g/L), spot glucose 5.2 mmol/L, 24-hour urine pro- tein 14 g.
(a) Should the amlodipine be changed to another drug in view of the ankle oedema?
(b) List 2 most relevant investigations.
(c) What is the clinical diagnosis, and the most likely renal histological diagnosis?
a) change to ACEI/ARB due to heavy proteinuria
b) renal biopsy, viral serology (HBsAg, anti HCV), autoimmune panel, serum and urine protein electrophoresis, malignancy screen
c) nephrotic syndrome, membranous nephropathy
Mr Chan, 31 years of age, developed progressive kidney failure from IgA nephropathy. He wondered if peritoneal dialysis (PD) would be suitable for him.
(a) What are the common contraindications to PD? Name 3.
He was eventually started on continuous ambulatory peritoneal dialysis (PD) with 3 bags of 1.5% (low strength) PD solutions per day. Over the course of the the ensuing five years, however, he developed several episodes of infective peritonitis, each time responding to treatment. At the latest follow up, he reported using 3 exchanges per day of 2.5% (medium strength) PD fluid plus one bag of icodextrin (7.5%).
(b) What is the most commonly used first-line treatment for CAPD peritonitis?
(c) Why do you think Mr Chan has required progressive higher doses of PD over the years? Name two possible reasons.
(d) Mr Chan’s 36-year-old brother volunteers to be a kidney donor. He has read from the Internet that IgAN runs in families, and seeks your advice whether he can be a kidney donor to his brother. What advice would you give him?
(e) Name 2 maintenance immunosuppressive agents that are commonly used in rejection prophy- laxis after kidney transplantation.
a) hernia, poor eye hand coordination, morbid obesity, multiple previous abd surgery
b) rapid exchanges x 3 bags with heparin. IP cefazolin + cefepine/gentamicin
c) repeated CAPD, prolong expsoure to dextrose leading to peritoneal membrane fibrosis
d) yes, but need extensive workup incl urinanalysis. However, still need extra workup to ensure suitability e.g. ABO, HLA
e) Inductive phase = ATG/Il2 + high dose steroid. Maintenance = steroid + CNI +MMF
a) hyperNa, hyperK, high urea/creatinine, sky high CK, low bicarbonate. Likely due to rhabdomyolysis
b) volume resuscitation by IV NS bolus 500ml/h first (shock kills first). IV bicarbonate after euvolemia to achieved forced alkaline diuresis (reduce renal toxicity of heme pigment), correction of electrolyte imbalance, dialysis if necessary
c) rhabdomyolysis
d) blood 3+ on dipstick but RBC -ve
a) membranous nephropathy
b) primary, drug induced (penicillamine, gold, NSAID, anti TNF), malignancy related (adenocarcinoma, CLL, paraproteinemia), autoimmune (seondary to lupus), viral infection (HBV, HIV, HCV)
c) malignancy screen (CXR, FOBT, SPE, PSA), autoimmune screen (ANA, anti dsDNA), HBsAg, anti HCV, anti HIV
d) AKI: RPGN Due to membranous nephropathy, drug related nephrotoxicity (e.g. calcineurin inhibitor), ARVO due to thrombotic tendency
Mr Chan, 34 years of age, developed ESRD from IgA nephropathy. A Tenckhoff catheter was placed and he was then started on continuous ambulatory peritoneal dialysis with 3 bags of 1.5% (low strength) PD solutions per day. Over the course of the next five years, however, he had several episodes of infective peritonitis, each time responding to treatment. At the latest follow up, he reported using 4 exchanges per day of 2.5% (medium strength) PD fluid.
(a) What are the common aetiological agents for CAPD peritonitis? Name 3.
(b) What is the most commonly used first-line treatment for CAPD peritonitis?
(c) Why do you think Mr Chan has required progressively higher doses of PD over the years? Name one reason.
Mr Chan’s 36-year-old brother volunteers to be a kidney donor. He has read from the Internet that IgAN runs in families, and seeks your advice whether he can be a kidney donor to his brother.
(d) What advice would you give him?
(e) Name 2 maintenance immunosuppressive agents that are commonly used in rejection prophy- laxis after kidney transplantation.
a) coagulase negative staphylococcus (epidermidis and haemolyticus), other gram+ve e.g. streptococcus, s. aureus.
b) rapid flush 3 bags PD fluid with heparin. Ultrafiltration. Intraperitoneal cefazolin + cefepime/gentamicin
c) prolonged PD –> peritoneal membrane fibrosis, esp with repeated CAPD peritonitis
d) Can. Needs detailed workup incl urinanalysis for RBC, even renal Bx. Also advice to carefully consider the risks of being a donor. Also inform that extensive workup needed to ascertain suitability (e.g. HLA)
e) Steroid, calcineurin inhibitor (tacrolimus), antimetabolite (MMF) most common combination
A 19-year-old student presents with a 2-week history of progressive facial swelling, worst upon awak- ening which gradually improves throughout the day. She has also noticed some swelling of there ankles over the last 3 days and that her urine has become quite frothy. She has no past medical illness and is not taking any medications. On examination, she is slim, comfortable and afebrile. BP is
110/67 mmHg. There is mild periorbital and pitting ankle oedema to mid shins. Examination is other- wise unremarkable. Investigations show: urine dipstick 4+ for albumin, but negative for blood, nitrites and glucose; serum albumin 18 g/dL; serum urea and creatinine 4 mmol/L and 50 umol/L, respectively.
24 hour urine protein 5.0 g. Renal ultrasound: no obstruction.
(a)What is the clinical diagnosis?
(b) What are the cardinal features of this condition?
(c) Name 3 potential complications of this condition.
(d) What investigation should be performed to ascertain a definitive diagnosis?
(e) What is the most likely definitive diagnosis in this patient?
(f) What pharmacologic treatment is likely to induce disease remission?
(a) nephrotic syndrome
(b) proteinuria >3.5g/d, albumin < 30g/L, edema, hyperlipidemia or lipiduria
(c) Infection, thromboembolism, protein malnutrition
(d) renal biopsy
(e) minimal change disease due to abrupt onset and age
(f) high dose oral steroid 1mg/kg/d
(a) marginal renal function deu to diuretic, ACEI. HyperK due to margin renal function, ACEI, MRA + K supplement
(b)
Immediate mx due to dangerous hyperK >6. Recheck K.
ECG state, cardiac monitor. BP/P, RR, SpO2 q4h, low K diet.
Stop ramipril, spironolactone, slow K
IV calcium gluconate for cardioprotection
DI drip in a separate line, bicarbonate if acidotic, nebulized ventolin is rarely used
Resonium A/C. Increase loop diuretic dose. Urgent dialysis if refractory
Long term after K normalize, restart ACEI at lower dose. Off K. Reconsider indication for MRA. Consider alternative e.g. ivabradine, CRT-D to optimize HF symptom control if needed. Regular serum K and RFT monitoring.
(a) hyperCa, hypoP, high ALP, renal impairment (high urea/creatinine)
b +c) PTHrP from CA lung leading to hyperCa and resulting prerenal failure from nephrotic DI. Bone met unlikely due to low phosphate
d) Strict IO, fluid intake at UO +500ml
ECG monitoring, BP/P RR SpO2 q4h
IV fluid + loop diuretics, IV bisphosphonate or IM calcitonin
PO Sandoz-phosphate
Consider dialysis with low calcium dialysate if refractory
(a) APO deu to AKI as evidenced by very high creatinine, high normal K, metabolic acidosis with respiratory compensation
(b) ACEI, NSAID precipitate AKI. Metformin: lactic acidosis with renal impairment
(c) serum lactate, >4mmol/L
(d) stop metformin immediately. Urgent dialysis indicated due to acidosis. IV NaHCO3- not indicated (done if pH< 7.1, HCO3< 6)
(a) lupus serology (ANA, anti dsDNA, C3,C4), clotting profile before assay
(b) lupus nephritis: explains anemia, hypoalbuminemia may be contributed to by protein losing enteropathy.
Primary membranous nephropathy: most common cause of nephrotic syndrome in adults, but doesnt explain mild anemia. Primary FSGS: 2nd most common cause.
(a) hyponatremia
(b) thiazide (renal loss), fluoxetine (SIADH), digoxin (digoxin toxicity exacerbated by lowish K), codeine (CNS suppression)
c) paired urine/plasma omsolarity, urine Na, CT brain, blood x CBC, LFT, TFT, CaPO4. Urinanalysis, C/ST, toxicology
(d) stop exacerbating drugs, assess volume status
If hypovolemic then replace by IV NS, while not exceeding daily limit of 10mmol/L. NS 500ml/h until BP normal. Calculate Na deficit by 0.6x BW x (serum Na -ideal Na).
Otherwise fluid restriction to 1L/d, high salt diet >8g/d.
(a) ddx: lupus nephritis, IgAN, PSGN, MPGN
ECG stat for any hyperK changes
Fluid restriction, low salt diet, vitals q4h
Ix
* ANA, anti dsDNA, C3/4 (HIV, HCV, HBV, ASLO, Ig pattern)
* Clotting before renal biopsy
* Blood culture
* Peripheral blood smear
* Bone marrow biopsy to r/o production defect
* Urine protein quantification
b) SLE, IgAN with underlying BM defect
