Salam,
Just nak share sikit adegan exam IM hari tu. Dah tak ingat sgt kes dia mcmana sebenarnya, sbb tak terfikir nak ambik balik clerking sheet masa exam hari tu. Tp, nak share jugak apa yg ingat... secara ringkasnya (mungkin ada yg dah alter2 sikit mana yg tak ingat)
Long Case IM – ESRF 2’ to GN
35/M/Female – ESRF came for training of self-CAPD
Date of exam:25th August 2010
Patient’s 1st problem arose during the pregnancy of her 1st child – she had persistent proteinuria but otherwise was symptomless. The pregnancy continued uneventfully & she delivered a healthy baby.
During her 2nd pregnancy about 2 years later, her pregnancy was complicated by persistent proteinuria & high BP. Renal profile was assessed and she was informed that her renal function was deteriorating. She was counselled for termination of pregnancy but on further discussion with O&G specialist, they allowed her to continue the pregnancy with close observation. She had multiple admissions for BP stabilization but did not need dialysis then.
After delivery of her 2nd child, her HPT persisted and renal function remained abnormal. She was advised for permanent contraception and kept under close follow-up with nephrology clinic every 2 monthly. However, she defaulted follow-up since 6 months ago (since Feb 2010) and resorted to traditional medicine instead.
About 1 month ago prior to admission, she presented with nausea, vomiting, lethargy, generalized pruritus and diarrhoea. She consulted a private Dr in which her renal profile was taken and she was told her renal function has further deteriorated. Out of worry, she went to A&E in which she was immediately treated for high potassium level and later admitted for further Mx.
Hx to rule out causes of renal failure:
Otherwise, she denied any oral ulcer, joint pain, alopecia, development of rashes, etc (TRO SLE).
Patient has no DM but has HPT.
No h/o fever a/w sore throat or pharyngitis prior to onset of Sx (TRO post-streptococcal GN)
No FxHx of polycystic kidney disease, autoimmune disease, or malignancy.
Hx to rule out Cx or decompensated renal failure: No SOB, no reduction of urine output, no leg swelling
(masa tu tak ingat sgt causes of renal failure, jadi Hx sgt tak lengkap)
Lalu bermulalah sesi soal jawab:
Dr: Why do you think pt presented with all those Sx (nausea, vomiting, lethargy, generalized pruritus and diarrhoea)?
Me: Uraemia
Dr: Do you think HPT came 1st in this patient or renal failure?
Me: HPT is secondary to renal failure
Dr: Why?
Me: This patient was Dx to have renal problem before she had the onset of HPT
Dr: For HPT to cause renal failure, it has to take years, at least 20 years or so. Only 4-5 years history of HPT is very unlikely to cause renal failure.
Dr komen: You forgot to ask 1 important question. I want to know whether she was counselled for renal biopsy?
Me: I forgot to ask. Bila tanya balik, rupanya she was counselled for renal biopsy in Feb 2010 and THAT was the actual reason for defaulting Rx & follow-up (she was scared!)
Dr: What do you think is the cause of ESRF in this patient?
Me: It can be due to SLE, but she has no symptoms of SLE in the history. It can also be due to GN.
Dr: What are types of glomerulonephritis that you know?
Me: Minimal change GN, Membranous GN, Focal segmental GN, Rapid Progressive GN
Dr: Which do you think is the type of GN in this patient?
Me: It can be membranous GN which is more common in adult than minimal change GN which is commoner in children.
Dr: What are the causes of MCGN? What are the causes of membranous GN?
Me: Infection, e.g. Malaria
Dr: Which type of malaria?
Me: Plasmodium malariae
Dr: What else are the causes of membranous GN?
Me: Errr.. (ada ke yg causes specific utk membranous GN? Tak baca laa)
Dr: Come on, very common in childhood.
Me: Post-streptococcal AGN
Dr: OK, what else?
Me: Em, SLE.
Dr: Yes, what else? What other autoimmune disease can cause membranous GN? What kind of malignancy can cause membranous GN?
Me: (dalam hati: Alamak, tak baca pulak pasal specific type of GN ni...)
Dr: Hmm, it’s OK, I just assume you don’t read. What causes RPGN?
Me: (dalam hati: yang ingat Wegener’s granulomatosis je, Dr Che Rosli pernah ajar and pernah lukis kat kelas... Tapi kalau aku ckp kang, Dr tanya apa tu Wegener’s, habislah aku tak tau jawab). Em, can SLE cause RPGN?
Dr: Yes, what else?
Me: Hmmm... (tengok lantai, kerutkan dahi)
Dr: It’s common in Chinese.
Me: ?????
Dr: Nevermind. It doesn’t matter. OK. What Ix do you want to do?
Me: FBC – CKD can result in anaemia.
Dr: What type of anaemia do you expect in CKD patient?
Me: It can be normochromic normocytic anaemia due to lack of erythropoietin. It can also be hypochromic microcytic due to anaemia of chronic disease & IDA.
Dr: Why CKD can result in IDA?
Me: It can be due to loss of appetite and poor oral intake. It can also be due to chronic blood loss.
Dr: Why CKD result in blood loss?
Me: Because CKD can cause platelet dysfunction.
Dr: Why CKD causes platelet dysfunction?
Me: Uraemia
Dr: Angguk. From where usually the blood is lost?
Me: Uraemic gastritis
Dr: Angguk, through the GIT. What other Ix do you want to do?
Me: I want to assess the renal function by doing renal profile
Dr: What do you expect the result will be?
Me: CKD usually results in proportionate increase in urea:creatinine ratio
Dr: What else?
Me: increase in uric acid and potassium due to reduce excretion
Dr: What other blood Ix do you want to do?
Me: Serum Ca
Dr: What do you expect the Ca will be in this patient?
Me: High
Dr: (terbelalak mata) HIGH???
Me: In the late stages patient may get hyperPTH and as a result, hypercalcemia
Dr: Secondary or tertiary hyperPTH?
Me: Tertiary
Dr: What happens in tertiary hyperPTH?
Me: The PTH gland secretes PTH (autonomously) regardless of the serum Ca.
Dr: What happens to the PTH gland?
Me: Hypertrophy
Dr: Hyperplasia. What else do you want to do?
Me: I would like to rule out the causes of GN in this patient. I want to screen for SLE.
Dr: What do you want to send?
Me: ANA & C3/C4 level.
Dr: What else?
Me: ASOT
Dr: What else do you want to do?
Me: Can we do ultrasound of the kidney?
Dr: What do you want to look for?
Me: Firstly, the size of the kidney (normal size 9-12cm).
Dr: So, you want to do renal US. If the size of kidney is still N, we can proceed with renal biopsy. If the size of kidney is 6cm would you proceed with biopsy?
Me: Errr (tak sure), no.
Dr: Correct, if the kidney size is still normal, we can still do renal biopsy to look for the cause of renal failure, e.g. GN and the specific type to treat accordingly. But if the kidney size is less than N, we don’t proceed with biopsy because the kidney is no longer salvageable. No use doing renal biopsy, we just proceed with dialysis.
Me: Ohh (macam tengah teaching pulak rasanya)
Dr: What are the causes of renal failure with a normal or enlarged kidney?
Me: Polycystic kidney
Dr: What else? More common.
Me: Diabetic nephropathy.
Dr: Ok. So how do you treat membranous GN?
Me: First we can try by giving steroids.
Dr: Will it respond to steroid?
Me: Not as good as MCGN. Only 20% responds to steroids.
Dr: Yes, but you still treat right. What is the catheter in patient’s neck?
Me: Internal jugular catheter.
Dr: What is it for?
Me: Haemodyalisis
Dr: Ok, so patient had haemodyalisis before. Now they are training her for CAPD. Tell me the Cx of CAPD and then we can go.
Me: Infection
