ASSIGNMENT 2

Michael, aged 42 years was seen by you 4 weeks ago for acute gastroenteritis and was noted
to have a B/P 155/ 95mm Hg. He has returned today to have a reassessment of blood
pressure. Now, feels perfectly well. His resting B/P is 148/ 85mmHg. He has a mild pitting
ankle oedema, a urine dipstick reveals 4+ protein and a moderate amount of blood. Clinical
examination is otherwise normal.

Biochemical tests:
- Urea 15mmol/l[3.3-7.3]
- Uric acid 580 mmol/l[209-431]
- Creatinine 160 umol/l [62-115]
- eGFR 50ml/min/1.73 mm
- Albumin 25 g/l[35-50]
- Cholesterol 6.8 mmol/l[ <5.2]
- Quantitation of total protein excretion yields 4.5 g/day

Question 1:
Assuming Michael's kidney disease is chronic [ > 3 months duration] , what stageis his CKD?
As above history, Michaels eGFR is 50 where he suffering from CKD stage 3A.
STAGES OF CHRONIC KIDNEY DISEASE
STAGE DESCRIPTION GFR
(mL/min/1.73m2)
1 Kidney damage with normal or increased >89
GFR
2 Kidney damage with mild reduced GFR 60-89
3A Moderately reduced GFR 45-59
3B Moderately reduced GFR 30-40
4 Severely reduced GFR 15-29
5 Kidney failure <15 or dialysis

(Ref: http://www.racgp.org.au/your-practice/guidelines/national-guide/chronic-kidney-
disease-prevention-and-management/)

Question 2:
What are the common and most likely causes of Michael's kidney disease?
Michaels kidney disease may be can be due to presents of :
1) Hypertension
- elevated pressure leads to damage of blood vessels within the kidney, as well as
throughout the body. This damage impairs the kidney's ability to filter fluid and
waste from the blood, leading to an increase of fluid volume in the bloodthus
causing an increase in blood pressure.
 2) Excessive proteinuria
- Proteinuria accelerates the rate of decline of GFR in hypertensive, diabetic, and
non-diabetic individuals. Hypertension exacerbates proteinuria and promotes
tubulointerstitial inflammation, fibrosis, and tubular atrophy, further elevating
blood pressure.

3) Hyperuricemia
- hyperuricemia associated with hyperuricosuria has been postulated to cause
kidney disease by depositing intraluminal crystal in the collecting duct of the
nephron

Question 3:
What are the likely complications which may arise from Michael's kidney disease?
1) Anemia
- Anemia of CKD usually begins during CKD Stage 3. The primary reason for
anemia in CKD is an absolute or relative deficiency of renal erythropoietin (EPO)
synthesis .

2) Bone disease and high phosphorus (hyperphosphatemia)

- Renal osteodystrophy is the spectrum of histological changes, which occur in bone
architecture of patients with CKD. The kidney is the primary site for phosphate
excretion and 1--hydroxylation of vitamin D. CKD patients develop
hyperphosphatemia as a result of inadequate 1, 25 dihydroxy-vitamin D levels that
reflect reduced synthesis from parenchymal scarring. In addition, renal phosphate
excretion is reduced. Together both processes cause, serum calcium levels to fall
resulting in increased secretion of parathyroid hormone .

3) Heart Disease
- Several cardiovascular risk factors associated with CKD are unique to patients
with this disease (non-traditional risk factors). Anemia, which has been discussed
above, is a risk factor for adverse cardiovascular outcomes in CKD patients.
Abnormal serum phosphate levels, calcium-phosphate ion product, and
parathyroid hormone levels are independent cardiovascular risk factors in the
setting of stage 5 CKD . Higher calciumphosphate products and the cumulative
dose of oral calcium-based phosphate binders correlate with the extent and
progression of arterial calcification

4) Hyperkalemia
- can impair the heart's ability to function and may be life-threatening

5) Fluid accumulation
- Healthy kidneys take out extra fluid (liquid) from your blood. When your kidneys
are not working as well as they should, they cannot take out enough fluid. This
can cause the extra fluid in your blood to build up in your body.

Question 4:
What treatment would you commence?

Question 5:
What is your next line of management for this patient?

Question 6:
Should Michael's hyperuricaemia be treated?

Michaels hyperuricaemia should be treated to prevent further damage to kidney but at

the same time, need monitor renal profile accordingly. In general, xanthine oxidase
inhibitors such as allopurinol or febuxostat are the preferred agents to decrease uric
acid levels due to their effectiveness in both overproducers and undersecretors of uric
acid. Widely recommended to start with low dosages of allopurinol in patients with
CKD and slowly titrate it to an effective dose. Febuxostat, a nonpurine selective
xanthine oxidase inhibitor, has been shown to be safe and effective for decreasing
serum uric acid levels and represents a pharmacologic alternative to allopurinol in
hyperuricemic patients who are unable to tolerate allopurinol.