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1. Which of the following medications require dose reduction in CKD?
2. Metformin, according to current guidelines, cannot be used in which diabetic patients?
3. Which of the following is true? Most diabetic patients with CDK, are:
4. In CKD, HbA1c offers an accurate view of glycaemic control.
5. In advanced CKD, which of the following therapies are preferred?
Case Study 1
Patient: Mrs H.T. – 62 years old
- T2DM, hyperlipidaemia
- CKD (eGFR 45ml/min), heavy proteinuria (4g daily), diabetic retinopathy
- Clinically: BMI 33, BP 132/76, HbA1c 7.4
- Metformin 500mg bd
- Glargine 24u daily
- Losartan 100mg
- Amlodipine 10mg
- Doxazocin XL 4mg
- Atorvastatin 10mg
- Disprin 150mg
Followed up 3 monthly
1 year later:
- eGFR 28ml/min
- Metformin stopped. HbA1c 6.2%. Glargine reduced to 20u daily.
- Gradual deterioration in eGFR. Admitted with pneumonia 1 year later: eGFR 8ml/min, HGTs normal in ward, HbA1c 5.4. All diabetic medication stopped.
- Stenotrophomonas maltophilia cultured from sputum. Started on oral co-trimoxazole. Patient noted to be unresponsive in the ward: HGT 2.3mmol.
- IV glucose restores consciousness, but persistent hypoglycaemic episodes.
- Co-trimoxazole changed to moxifloxacin: patient made a good clinical response and discharged on glulisine for glycaemic control.
- Persistent low eGFR of 8ml/min and fluid overload: patient started on peritoneal dialysis.
6. The heavy proteinuria related to diabetes should lead us to expect a relentless progressive course in her kidney disease?
View Expert Comment »
This patient has heavy proteinuria, which is a risk marker for a relentlessly progressive course in her kidney disease, and should prompt early referral to a nephrologist. She would need more frequent monitoring of her renal function, as well as glycaemia control, with more frequent adjustments of her diabetic medication in order to avoid hypoglycaemia.
7. The patient’s eGFR was 8ml/min by the time the glargine was stopped, when should it have been stopped?
8. Co-trimoxazole needs to be used with caution in renal failure because:
9. What is the most appropriate therapy at discharge?
View Expert Comment »
Because of the reduced clearance of insulin in chronic kidney disease, the patient is able to maintain a low HbA1c with little or no diabetic medication. This will most likely translate to good fasting blood glucose levels, but the patient may still experience post-prandial peaks due to the blunted pancreatic beta cell response to hyperglycaemia at mealtimes. With such a low HbA1c, the patient clearly does not need exogenous basal insulin, but may still require some bolus insulin if peaking post-prandially.
Case Study 2
Patient: Mr R.B. – 59 years old
- T2DM, hypertensive, hyperlipidaemia, central obesity
- Aortic valve replacement aged 13 years
- ESRD on HD since April 2016
- Severe secondary hyperparathyroidism and hyperkalaemia
- NPH insulin 30u daily
- Lisinopril 20mg
- Indapamide 2.5mg
- Carvedilol 25mg bd
- Moxonidine 0.3mg
- Simvastatin 20mg
- Disprin 100mg
- Allopurinol 300mg
Assessed for parathyroidectomy
Date Weight BP Dipstix HbA1c 13/12/2013 120kg 132/90 3+ protein 6.1 19/09/2014 108kg 147/90 3+ protein 6.6 04/12/2015 110.5kg 142/90 3+ protein 6.4 01/11/2016 108kg 128/82 Bladder empty 5.8 Date Urea Creatinine eGFR HbA1c Insulin dose 30/03/2012 17.8 231 27.4 Biosulin N 30u 15/02/2013 24.1 292 20.8 30u 11/03/2015 14.4 30u 08/08/2015 14.1 30u 14/03/2014 25.4 342 17.2 30u 07/01/2015 16.5 311 18 30u 08/09/2015 24 349 15 30u 04/04/2016 34.8 653 7 11.9 0 06/05/2016 22.7 583 7 10.5 0
10. Was the BP therapy adequate?
View Expert Comment »
Given that the patient had systolic BP in excess of 140mmHg, his BP control was not adequate. South African Hypertension Society Guidelines recommend a BP target of <140/90 mmHg regardless of CV risk and co-morbidities. KDIGO guidelines recommend a target equal to or less than 140/90mmHg for diabetic patients with CKD whose urine albumin excretion is less than 30mg per 24 hours. For the diabetic patient with CKD who has a urine albumin excretion greater than 30mg per 24 hours, they recommend a target equal to or less than 130/80mmHg.
11. Is the HbA1c fairly accurate in the range of 6-7% in the setting of CKD?
View Expert Comment »
HbA1c as a marker of glycaemic control may often be unreliable in the setting of ESRD. However, data have shown that an HbA1c in the range of 6-7% still remains fairly accurate. If home BG readings appear to contradict HbA1c readings, then the HbA1c readings should be interpreted with caution.
12. Does the persistent need for unchanged insulin dose until well into advanced CKD reflect the uraemia-induced insulin resistance?
View Expert Comment »
DeFronzo and others found that tissue insensitivity to insulin is the primary cause of uremic-induced insulin resistance. In their study, uremic subjects’ insulin-mediated glucose metabolism was reduced by 47% versus non-uremic controls.
Case Study 3
Patient: Mrs B.W. – 58 years old
- T2DM for 10 years
- Rx: Gliclazide MR 120mg daily, metformin 1g bd
- Minimal SMBG, occasional hypo symptoms
- Co-morbidities: Hypertension, HL, CAD with 2 stents, obesity, ESRD
- Weight 109kg
- BMI 43
- HGT 5.1mmol
- HbA1c 7.3%, Creatinine 336, proteinuria
– ineligible for oral agents
– needs insulin Rx
– prolonged insulin half-life with lower dose requirement
– insulin resistant (BMI 43)
- Begin regular SMBG, refer to DNE for education
- Refer to renal practice
- Start insulin (stopped oral agents)
Insulin dose calculation (with renal failure, dose should be less than usual BUT with a very high BMI, dose may be more than usual)
For this patient: estimated TDD = 0.1-1.2u x 109kg = 11-131u daily
- Discontinue metformin, gliclazide
- Glargine 4u commenced in the morning (started at such a low dose to allow SU to washout, given mane to reduce risk of nocturnal hypos)
- Monitored to up titrate glargine, and aspartate supplementary scale added before meals
- Final dose: Glargine 20u mane, 11u nocte
Aspartate supplementary scale 3-7u before meals
Renal, obesity adjusted TDD ~ 45u/ day (0.4u/kg)
13. Given this patient’s insulin resistance, it would have been acceptable to continue with the gliclazide.
14. What would the status of the patient’s resistance have been earlier in the course of her renal impairment?
15. Given her obesity, what other therapy could have been considered?
- Tuttle KR, Bakris GL, Bilous RW, et al. Diabetic kidney disease: a report from an ADA Consensus Conference. Diabetes Care 2014; 37(10): 2864-2883.
- Pecoits-Filho R, Abensur H, Betonico CCR, et al. Interactions between kidney disease and diabetes: dangerous liaisons. Diabetol Metab Syndr 2016; 8: 50.
- Toth-Manikowski S and Atta MG. Diabetic Kidney Disease: Pathophysiology and Therapeutic Targets. J Diabetes Res 2015; 2015: Article ID 697010. doi:10.1155/2015/697010.
- Iyer SN and Tanenberg RJ. Managing diabetes in hospitalized patients with chronic kidney disease. Clevelend Clinic J Med 2016; 83(4): 301-310.
- Hahr AJ and Molith ME. Management of diabetes mellitus in patients with chronic disease. Clin Diab Endocrinol 2015; 1: 2.
- Hill NR, Fatoba ST, Oke JL, et al. Global Prevalence of Chronic Kidney Disease – A Systematic Review and Meta-Analysis. PLOS One 2016; 11(7): e0158765. doi: 10.1371/journal.pone.0158765.
- Alsahli M and Gerich JE. Hypoglycemia in Patients with Diabetes and Renal Disease. J Clin Med 2015; 4(5): 948-964.
- Moen MF, Zhan M, Hsu VD, et al. Frequency of hypoglycemia and its significance in chronic kidney disease. Clin J Am Soc Nephrol 2009; 4(6): 1121-7.
- CKD Workgroup. Kidney disease: Improving global outcomes (KDIGO) CKD work group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Inter Suppl 2013; 3: 1-150.
- Levey AS, de Jong PE, Coresh J, et al. The definition, classification, and prognosis of chronic kidney disease: a KDIGO Controversies Conference report. Kidney Int 2011; 80(1): 17-28. doi: 10.1038/ki.2010.483.
- Iglesias P and Diez JJ. Insulin therapy in renal disease. Diab Ob Metab 2008; 10: 811-823.
- Mak RH. Insulin resistance in uremia: effect of dialysis modality. Pediatric Res 1996; 40(2): 304-8.
- Sampanis CH. Management of hyperglycemia in patients with diabetes mellitus and chronic renal failure. Hippokratia 2008; 12(1): 22-27.
- Mak RH. Impact of end-stage renal disease and dialysis on glycemic control. Semin Dial 2000; 13(1): 4-8.
- Mak RH and DeFronzo RA. Glucose and insulin metabolism in uremia. Nephron 1992; 61(4): 377-82.
- Inzucchi S, Lipska JA, Mayo H, et al. Metformin in patients with type 2 diabetes and kidney disease: a systematic review. JAMA 2014; 312(24): 2668-2675.
- Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. N Engl J Med 2015; 373(22): 2117-28. doi: 10.1056/NEJMoa1504720.
- Wanner C, Inzucchi SE, Lachin JM, et al. Epagliflozin and progression of Kidney Desease in Type 2 Diabetes. N Engl J Med 2016; 375(18): 1800-1.
- Marso SP, Daniels GH, Brown-Frandsen K, et al. Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes. N Engl J Med 2016; 375(4): 311-22.
- Mann JF. ADA 76th Scientific Sessions, Session 3-CT-SY24. June 13 2016, New Orleans, LA.
- Hasslacher C, Kulozik F and Bermejo JL. Treatment with insulin analogs, especially Glargine and Lispro, associates with better renal function and higher hemoglobin levels in Type 1 diabetic patients with impaired kidney function. Ther Adv Endocrinol Metab 2016; 7(4): 166-177.