Nephrology Flashcards
Renal transplant on immunosuppression
presented with visual hallucinations
Which drug
Mycophenolate mofetil
Azathioprine
Prednisolone
Tacrolimus
Ciclosporin
Prednisolone
Steroid:
psychosis, weight gain, secondary diabetes, osteoporosis and myopathy.
Ciclosporin:
nephrotoxicity, gum hypertrophy and hirsutism
Tacrolimus:
tremor and secondary diabetes
Mycophenolate mofetil:
mucositis
Azathioprine:
rashes, hepatitis and pancreatitis.
Chronic kidney disease: hypertension management
The majority of patients with CKD will require more than two drugs to treat hypertension. ACE inhibitors are first line and are particularly helpful in proteinuric renal disease (e.g. diabetic nephropathy).
NICE suggest that:
- Decrease in eGFR of up to 25% or
- Rise in creatinine of up to 30% is acceptable,
Furosemide is useful as a anti-hypertensive in patients with CKD, particularly when the GFR falls to below 45 ml/min*. It has the added benefit of lowering serum potassium.
Pre-renal
Renal
Post-renal
(Urine Na and Osmolarity)
Prerenal AKI:
This is typically due to reduced renal perfusion. In this context, the kidneys conserve sodium to maintain intravascular volume. Therefore, you would expect:
- Low urinary sodium concentration: Generally <20 mmol/L.
- High urinary osmolality: Usually >500 mOsm/kg, indicating concentrated urine as a response to perceived hypovolaemia.
Renal AKI (e.g., ATN):
In this scenario, tubular function is impaired, leading to less effective sodium reabsorption. Consequently, you would observe:
- High urinary sodium concentration: Typically >40 mmol/L.
- Low urinary osmolality: Often <350 mOsm/kg, reflecting the inability to concentrate urine due to tubular damage.
Post-renal AKI:
Urinary Sodium: Variable, but can be low or normal depending on the duration of obstruction and compensatory mechanisms.
- Urinary Osmolality: Often low (<350 mOsm/kg) if there is prolonged obstruction, reflecting impaired concentrating ability.
On examination, he was comfortable at rest but had marked pitting oedema of both lower limbs and bilateral dullness to percussion at the lung bases. His blood pressure was 181/101mmHg.
Urine dipstick showed 2+ blood and 4+ protein.
Blood test results were as follows:
Urea 21 mmol/L (2.0 - 7.0)
Creatinine 256 µmol/L (55 - 120)
Albumin 24 g/L (35 - 50)
24-hour urine protein was measured to be 8g/day.
Further blood tests were carried out:
ANA negative
ANCA negative
Complement (C3 and C4) negative
Hepatitis serology negative
HIV screening serology negative
Serum protein electrophoresis negative
A renal ultrasound was performed:
Left kidney 10.8cm, right kidney 11.3cm. There is an increased echogenicity bilaterally. No hydronephrosis is present. Peak flow velocities normal and equal bilaterally.
A renal biopsy was performed:
There are segmental areas of scarring affecting some of the glomeruli. No hypercellularity or crescents can be seen.
How should this patient be managed given the likely diagnosis?
Causes
idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport’s syndrome
sickle-cell
Focal segmental glomerulosclerosis is noted for having a high recurrence rate in renal transplants.
Investigations
renal biopsy
focal and segmental sclerosis and hyalinosis on light microscopy
effacement of foot processes on electron microscopy
Management
steroids +/- immunosuppressants
Prognosis
untreated FSGS has a < 10% chance of spontaneous remission
DVT give DOAC unless:
Renal failure
Antiphospholipid
Give
LMWH or UFH + Warfarin
Erythropoietic stimulating agent (ESA) and Ferritin in CKD
A ferritin of >100 is required prior to initiation of an ESA
