Diabetes is associated with markedly increased cardiovascular risk, a risk compounded with imposition of chronic kidney disease (CKD). More than 80% of people with diabetes and CKD have hypertension, and many have an obliterated nocturnal blood pressure “dip,” the normal physiological drop in blood pressure during sleep. Appropriate blood pressure measurement is the Achilles heel of hypertension management, especially in diabetic kidney disease (DKD).

1. Management of Hypertension in Diabetic Patients with
Chronic Kidney Disease: A pathologist perspective view
Dr.Osbourne .E.Nyandiva
FACULTY OF HEALTH SCIENCE
SCHOOL OF MEDICINE

2. INTRODUCTION
Diabetes is associated with markedly increased
cardiovascular risk, a risk compounded with imposition of
chronic kidney disease (CKD). More than 80% of people with
diabetes and CKD have hypertension, and many have an
obliterated nocturnal blood pressure “dip,” the normal
physiological drop in blood pressure during sleep.
Appropriate blood pressure measurement is the Achilles heel
of hypertension management, especially in diabetic kidney
disease (DKD).

3. • The prevalence of kidney disease and diabetes is
increasing among the people of the Pacific with an
unknown proportion having metabolic syndrome. The
preponderance of those with diabetic kidney disease
(DKD) will not progress to kidney failure, but rather will
succumb to cardiovascular disease (CVD).
•

4. PATHOPHYSIOLOGY........
• Hypertension in CKD is marked by extracellular fluid volume
expansion, sympathetic nervous system activation, and
vasoconstrictor accumulations of endothelin and
asymmetric dimethylarginine, an endogenous nitric oxide
inhibitor. Salt sensitivity is common.

5. • The prevalence of “non-dipping,” the absence of the
naturally occurring blood pressure decline during sleep,
increases as CKD worsens from 15% in normal subjects to
75% in those with kidney failure (CKD Stage 5). In CKD, a
linear correlation exists between hypertension and
progressive kidney damage; blood pressure control is
crucial to slowing the progression of CKD. Diabetes is also
associated with increased arterial stiffness from accelerated
atherosclerosis, in part the consequence of increased
protein glycation attributable to suboptimal glycemic control.

6. Evaluation of Hypertensive Patients
 A careful patient history includes the following:
 Duration of hypertension
 Previously used medications
 Review of adverse drug side effects, allergies, or
intolerances
 Identification of social/support networks (isolation decreases
medication adherence)
 Smoking, alcohol, or drug history

7.  Current medication reconciliation (reviewing pill bottles and
counts to confirm that the patient is taking medications as
directed) that includes use of complementary and over-the-
counter drugs that may increase blood pressure
 Menstrual history (i.e., oligomenorrhea from polycystic ovary
syndrome
 Exercise and dietary history, including sodium, calcium, and
potassium intake
 Screening for obstructive sleep apnea (Epworth scale)
 Assessment of medication-taking behavior (i.e., adherence)

9. Arterial Hypertension in Chronic Kidney Disease

10. Prevalence of Hypertension in Renal Parenchymal Disease

11. Management of Hypertension in Chronic Kidney Disease
• Investigations into the nature of the patient’s renal
disease
• Blood pressure goal
• Non-pharmacological treatment
• Pharmacological treatment

12. JOINT NATIONAL COMMITTEE
CKD
SBP <140 mmHg DBP <90 mmHg
ACEI/ARB alone or in
combination with
other drug class

13. ESH/ESC
SBP <140 mmHg DBP <90 mmHg
CKD

14. ESH/ESC

15. KIDNEY DISEASE | IMPROVING GLOBAL OUTCOMES - KDIGO
• Non-diabetic adults with CKD:
≤140 mmHg systolic and ≤90 mmHg diastolic if normoalbuminuric
≤130 mmHg systolic and ≤80 mmHg diastolic if micro or macroalbuminuric
• Diabetic adults with non dialysis-dependent CKD:
≤140 mmHg systolic and ≤90 mmHg diastolic if normoalbuminuric
≤130 mmHg systolic and ≤80 mmHg diastolic if micro or macroalbuminuric
• Kidney transplant recipients:
≤130 mmHg systolic and ≤80 mmHg diastolic
• Elderly people with CKD:
probably ≤140 mmHg systolic and ≤90 mmHg diastolic, but set targets
after consideration of co-morbidities
Aim for <130/80 mmHg if albuminuria is present

16. Blood Pressure Goals in CKD
There is little evidence among patients with CKD that a BP goal
of less than 130/80mmHg saves lives, saves kidneys or
reduces cardiovascular events.
Nonetheless, BP control is important. Therefore, as in the
general population, BP should be targeted to less than
140/90mmHg.
Hypertension therapy personalized and individualized using
home BP monitoring holds great promise.

17. Blood Pressure Goals in CKD

18. Lifestyle Measures
• Weight:
Achieve or maintain a normal weight (BMI 20-25 kg/m²)
• Salt:
< 2 g sodium (5 g salt) per day unless contraindicated
• Exercise:
At least 30 minutes 5 times per week
• Alcohol:
Limit to maximum of 2 standard drinks per day
• Smoking:
No direct effect on long-term BP but cessation reduces CV risk.

19. Pharmacological Treatment

20. • Generalised arterial vasodilatation:
Reduction of blood pressure
• Vasodilatation particularly of the efferent glomerular arteriole:
Reduction of glomerular pressure
Reduction of proteinuria
Long-term renoprotection
• Reduction of adrenal aldosterone secretion:
But note aldosterone breakthrough
ACEIs and ARBs

21. ACEIs and ARBs
Indicated in all hypertensive patients with CKD, especially in proteinuric diabetic
and non-diabetic CKD.
Will lead to deterioration of renal function in short term but then to slower
progression of renal failure in longer term.
KEY POINTS TO ALL HEALTHCARE PROVIDER

22. Side Effects
Hyperkalaemia
Higher risk of hyperkalaemia in combination with potassium-sparing diuretics
ACEI: mainly renal excretion (except fosinopril, trandolapril), ARB mainly hepatic
excretion, therefore reduce dose (stop?) at GFR <15 mL/min
Other treatment strategies in Hyperkalaemia:
• Dietary advice
• Furosemide -used to treat fluid build-up due to heart failure, liver scarring, or kidney
disease. It may also be used for the treatment of high blood pressure
• Dose reduction of ACEI/ARB

23. Side Effects
AKI, especially in:
• Bilateral renal
stenosis
• Diabetes and
sepsis
• Combination with
NSAIDs
• State of volume
depletion
(diarrhoea/
vomiting)

24. It is premature to draw a definite conclusion as to whether aldosterone
antagonists—through their anti-albuminuric, anti-hypertensive, or anti-
fibrotic effects—reduce the rate of decline in kidney function in the long
term. This is an area for future research.
Aldosterone Antagonists

25. Often Combination Therapy will be Required

26. Pharmacological Treatment

27. Diuretics
Thiazide diuretics: e.g. Hydrochlorothiazide, Bendroflumethiazide
Thiazide-like diuretics: e.g. Chlorthalidone, Indapamide
Loop diuretics: e.g. Furosemide, Torasemide
Widely used as patients with CKD are characterised by sodium and water retention
For antihypertensive therapy:
GFR >50 mL/min: Thiazides alone or in combination with distal diuretics (e.g.
spironolactone)
GFR <30 mL/min: Loop diuretics. Avoid distal (potassium sparing) diuretics.

28. Calcium Channel Blockers
Antihypertensive action.
Oedema and fluid retention.
Dihydropyridines predominantly dilate the afferent arteriole and thereby increase
GFR but also the glomerular pressure.
Non-DHPs seem not to have this effect.

29. Calcium Channel Blockers

30. Beta-Blockers
Beta-blockers reduce increased sympathetic activity in CKD.
Indication in heart failure.
Often combined with diuretics in RCTs but no reason why not combine with
others.
No robust evidence for superiority of certain beta-blockers.

31. Alpha-Blockers
Alpha-blockers have additional antiproliferative properties.
Hepatic excretion.
Beneficial in prostate hypertrophy.