Diabetic Nephropathy Review

1. JAFAR AL-SAID. M.B.CHB. MD. FASN. FACP.
CHAIR OF INTERNAL MEDICINE.
NEPHROLOGY AND INTERNAL MEDICINE CONSULTANT.
BAHRAIN SPECIALIST HOSPITAL.
Diabetic Nephropathy
1Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

2. 2Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

3. 3Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

4. • Introduction.
• Epidemiology.
• Pathogenesis.
• Progression.
• Diagnosis.
• Management.
Scheme
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5. Historical Points
• 18th Century Proteinuria was recognized in DM.
• 1930 Kimmelstiel and Wilson described the typical nodular
glomerular lesion in Dm with Proteinuria.
• 1950 Kidney disease was recognized as DM complication.
• Current Leading cause of ESRD in USA and western societies.
BatumanVecihi, Khardori Romesh, et. Al. Diabetic Nephropathy: Background, Pathophysiology, Etiology
Medscape. Updated: Jul 31, 2015 5Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

6. 20-40% of DM patient will develop Nephropathy.
In the presence of Minimal Albuminuria > 300mg/dl It will develop in:
• 80% of DM I.
• 20-40% of DM II.
Introduction
Suma Dronavalli, Irena Duka, George L. Bakris. The Pathogenesis of Diabetic Nephropathy Posted: 08/01/2008; Nat
Clin Pract Endocrinol Metab CME © 2008. http://www.medscape.org/viewarticle/577156
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7. Definition
A syndrome characterized in diabetics by 2 of the following:
• Persistent albuminuria > 300mg/day. On at least to occasions 3 -6m apart.
• Progressive decline in GFR.
• Elevated BP.
BatumanVecihi, Khardori Romesh, et. Al. Diabetic Nephropathy: Background, Pathophysiology, Etiology
Medscape. Updated: Jul 31, 2015
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8. 71%
65%
44%
28.50%
0%
10%
20%
30%
40%
50%
60%
70%
80%
Hypertension Dyslipidemia Kidney Disease Blindness
Comorbid conditions
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9. Distribution of NHANES
participants with diabetes, self-
reported cardiovascular disease,
& single-sample markers of CKD,
2007-2012
Data Source: National Health and Nutrition
Examination Survey (NHANES), 1988–1994, 1999-
2004 & 2007–2012 participants aged 20 & older.
Cardiovascular disease designation is based on self-
report of any CVD.
CKD is defined as eGFR <60 or ACR ≥30.
Prevalence of Diabetic with CKD.
NHANES. Adults 2012.
USRDS 2015
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10. Prevalence of CKD by age &
risk factor among NHANES
participants,
1998-2012
National Health and Nutrition Examination
Survey (NHANES), 1988–1994, 1999-2004 &
2007–2012 participants aged 20 & older.
Diabetes defined as either HbA1c >7%, self-
reported, or currently taking glucose-
lowering medications.
Hypertension defined as BP ≥130/≥80 for
those with diabetes or CKD, otherwise BP
≥140/≥90, or taking medication for
hypertension.
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11. Distribution of markers of CKD in
NHANES participants with diabetes,
hypertension, self-reported
cardiovascular disease, & obesity,
2007–2012
National Health and Nutrition
Examination Survey (NHANES), 2007–
2012 participants aged 20 & older.
Single-sample estimates of eGFR &
ACR; eGFR calculated using the CKD-
EPI equation.
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12. Trends in annual number of
ESRD incident cases (in
thousands), by primary
cause of ESRD, in the U.S.
population, 1996-2013
ESRD Incidence
by cause
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13. ESRD prevalence
by cause
Trends in annual number of
prevalent ESRD cases (in
thousands), by primary
cause of ESRD, in the U.S.
population, 1996-2013
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14. Trends in adjusted*
prevalence (per million) of
ESRD,
by primary cause of ESRD, in
the U.S. population, 1996-
2013
ESRD Prevalence
per population
By cause
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15. Functional Structural ESRD
Progression
Hemodynamic
changes
Thickening of GBM.
Mesangial expiation.
Glom. hypertrophy
Irreversible Scarring
Hypertension.
Decreased eGFR.
Proteinuria.
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16. Microalbuminuria Macroalbuminuria?
Steinke JM et al. (2005) The early natural history of nephropathy in type 1 diabetes: III. Predictors of 5-year urinary
albumin excretion rate patterns in initially normoalbuminuric patients. Diabetes
54:2164-2171
Progression
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17. <30mg
Normal
30-
300mg
Moderate
>300m
g
Sever
Albuminuria as continuum value
Microalbuminuria
KDIGO Reference 22
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18. • Is a continuum.
• Varies according to:
• Time.
• Physical Activity.
• Fever.
• Blood pressure.
• Labs variation.
• Dietary Prot. intake.
Albuminuria
Tuttle K, Bakris G. et. al. Diabetic Kidney Disease: A Report From an ADA Consensus Conference. Diabetes Care
2014;37:2864–2883 | DOI: 10.2337/dc14-129 18Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

19. Hemodynamic
GeneticMetabolic
Factors Contributing to
development of Diabetic
Nephropathy
Nephropathy
Ziyadeh FN (2004) Mediators of diabetic renal
disease: the case for TGF-â as the major
mediator. J Am Soc Nephrol 15 (Suppl 1): S55-
S57
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20. Decreased
Resistance
Afferent > Efferent
Increased
intraglomerular
pressure
.Mechanical strain.
.Albumin leak.
Mesangial expansion.
.GBM thickness.
Podocytes injury
Hemodynamic Pathway
• Prostanoid.
• NO2.
• VEGF.
• RAAS.
• Endothilin.
• TGF-B1.
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21. PKC
Hyperglycemia Injury
Mesangial Matrix expansion.
Cell apoptosis.
Increased Podocyte Permeability
VEGF
TGFB1
Over
expression
GLUT 1,4
Friedman EA (1999) Advanced glycation endproducts in diabetic nephropathy. Nephrol Dial Transplant 14 (Suppl 3): S1-S9.
Porte D Jr and Schwartz (1996) MW Diabetes complications: why is glucose potentially toxic? Science 272: 699-700.
Brownlee M (2001) Biochemistry and molecular cell biology of diabetic complications. Nature 414: 813-820.
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22. Glycosylation End Products
Glucose
+
Amino A.
Proteins.
Advanced glycosylation
end products
Microvascular
Complications
Makita Z et al. (1991) Advanced glycosylation end products in patients with diabetic nephropathy.N Engl J Med 325: 836-842
Singh AK et al. (1998) Effect of glycated proteins on the matrix of glomerular epithelial cells. J Am Soc Nephrol 9: 802-81022Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

23. Protein Kinase C
Oxidative stress
DiacyglycerolHyperglycemia
Activation
PKC TGF B1
Mesangial
Expansion
GBM thickening
Yamagishi S et al. (2007) Molecular mechanisms of diabetic nephropathy and its therapeutic intervention.
Curr Drug Targets 8: 952-959
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24. TGF-B1
Hyperglycemia
Increase expression of
TGF-B1
Cellular Hypertrophy.
Collagen Synthesis
Sharma K et al. (1999) Captopril-induced reduction of serum levels of transforming growth factor-â1 correlates with long-
term renoprotection in insulindependent diabetic patients. Am J Kidney Dis. 34:818-823
Sharma K and Ziyadeh FN (1995) Hyperglycemia and diabetic kidney disease. The case for transforming growth factor-beta as
a key mediator. Diabetes 44: 1139-1146
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25. Pathogenesis of Diabetic Nephropathy
BatumanVecihi, Khardori Romesh, et. Al. Diabetic Nephropathy: Background, Pathophysiology, Etiology
Medscape. Updated: Jul 31, 2015
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26. • Diabetic Nephropathy is more common within first degree relatives.
Among Pima Indian developed Overt Proteinuria:
• 14 % neither parents had Proteinuria.
• 23% one parent had proteinuria.
• 46% both parents had proteinuria.
Genetic susceptibility
Trevisan R and Viberti G (1995) Genetic factors in the development of diabetic nephropathy. J Lab Clin Med 126:
342-349.
Pettitt DJ et al. (1990) Familial predisposition to renal disease in two generations of Pima Indians with type 2 (non-
insulin-dependent) diabetes mellitus. Diabetologia 33: 438-443.
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27. Susceptibility loci for Microvascular complication on Chromosomes:
3, 7, 9, 20.
Diabetic Nephropathy susceptible gene areas on chromosomes:
• 7q21.3
• 10p15.3
• 14q23.1
• 18q22.3
Genetic susceptibility
Imperatore G et al. (1998) Sib-pair linkage analysis for susceptibility genes for microvascular complications among Pima Indians with type 2 diabetes.
Pima Diabetes Genes Group. Diabetes 47: 821-830.
Vardarli I et al. (2002) Gene for susceptibility to diabetic nephropathy in type 2 diabetes maps to 18q223-23. Kidney Int 62: 2176-2183.
Iyengar SK et al. (2007) Genome-wide scans for diabetic nephropathy and albuminuria in multiethnic populations: the family investigation of
nephropathy and diabetes (FIND). Diabetes 56: 1577-1585
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28. Pathology
• ECM expansion.
• Mesangial expansion.
• Kimmelstiel-Wilson nodule.
• Arteriolar Hyalinosis.
• Glomerular sclerosis.
• Thickening of GBM.
• Thickening of TBM.
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29. DM
CVD
CKD
Which one started first ??
High CV risk patient
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30. DM + CKD
Coronary Art.
disease
CVD risk Assessment
=
Tonelli M, Muntner P, Lloyd A, et al.; Alberta
Kidney Disease Network. Risk of coronary events in
people with chronic kidney disease
compared with those with diabetes: a population
level cohort study. Lancet 2012;380:807–814
Atherosclerosis
AMI.
Cardiac fibrosis.
Art. Calcification. 30Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

31. • Absence of retinopathy.
• Rapid decrease eGFR.
• Rapidly increasing Proteinuria.
• Refractory HTN.
• Active urinary sediments.
• > 30% reduction of GFR with RAAS.
• Clinical picture for other systemic disease.
Increased possibility of causes other than DM leading
to the kidney disease:
National Kidney Foundation. KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations
for Diabetes and Chronic Kidney Disease. Am J Kidney Dis 2007;49(Suppl. 2) S12–S154
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32. 32Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

33. Management of Diabetic Nephropathy
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34. Multidisciplinary Approach
Internist
Nephrologist
Patient
Endocrinologist
Dietician
Social worker
Cardiologist
Nurse
Pharmacist
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35. • Lifestyle.
• BP.
• DM.
• Lipids.
• Depression.
• Compliance.
Managing Diabetic Nephropathy
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36. Certain points to be considered:
• Fluid intake.
• Salt intake. 5 gm daily. (Na 2.3 gm).
• Protein. Recommended 0.8gm/kg daily.
• Hyperkalemia.
• Acid/Base.
• Malnutrition.
• Anemia.
• PTH, Vit. D, Ca & PO4.
Dietary Remarks in Diabetic Kidney Disease
Tuttle K., Bakris G. Diabetic Kidney Disease: A report from an ADA Consensus. Diabetes Care. Vol. 37, Oct 2014
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37. Target BP in Diabetic patient
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38. Target BP < 140/90mmHg in diabetic CKD.
< 130/80mmHg with Alb./Creat. > 30mg/day
Diastolic < 60mmHg was associated with higher ESRD.
Diastolic < 65mmHg was associated with poor CV outcome.
Hypertension in Diabetic patients
• Wheeler DC, Becker GJ. Summary of KDIGO guideline. What do we really know about management of blood pressure in patients with chronic
kidney disease? Kidney Int 2013;83: 377–383
• James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel
members appointed to the Eighth Joint National Committee (JNC 8). JAMA 2014;311: 507–520
Peralta CA, Norris KC, Li S, et al.; KEEP Investigators. Blood pressure components and end-stage renal disease in persons with chronic kidney disease:
the Kidney Early Evaluation Program (KEEP). Arch Intern Med 2012;172:41–47
Kovesdy CP, Bleyer AJ, Molnar MZ, et al. Blood pressure and mortality in U.S. veterans with chronic kidney disease: a cohort study. Ann Intern Med
2013;159:233–24
38Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

39. • ACE inh. & ARB reduce the progression of kidney disease.
• This is specifically true in CKD III or higher with significant proteinuria.
• CONTRAINDICATED TO USE COMBINATION ACE inh. and ARB.
RAAS in CKD with DM
Fried LF, Emanuele N, Zhang JH, et al.; VA NEPHRON-D Investigators. Combined angiotensin inhibition for the treatment of
diabetic nephropathy. N Engl J Med 2013;369:1892–1903
Parving H-H, Brenner BM, McMurray JJV, et al.; ALTITUDE Investigators. Cardiorenal end points in a trial of aliskiren for type 2
diabetes. N Engl J Med 2012;367:2204–2213
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40. Department of Public Health and Clinical Medicine, Medicine, Umeå University, SE-901 87
Umeå, Sweden Correspondence to: M Brunström mattias.brunstrom@umu.se Additional material is published
online only. To view please visit the journal online. Cite this as: BMJ 2016;352:i717
http://dx.doi.org/10.1136/bmj.i717. Accepted: 12 January 2016
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41. Aim: Assess the CV mortality and morbidity in DM with different BP targets.
Design: Meta-analysis. (Central, Medline, Ebase, Biosis.)
Eligibility:
• RCT > 100 with DM.
• Treated for > 12 months.
• Comparing two agents.
• Two target BP.
• One versus two drugs.
Effect of antihypertensive treatment at different blood pressure levels in patients
with diabetes mellitus: systematic review and meta-analyses
BMJ 2016;352:i717 | doi: 10.1136/bmj.i717 41Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

42. Results:
49 Trials.
N = 73 738 participant.
Effect of antihypertensive treatment at different blood pressure levels in patients
with diabetes mellitus: systematic review and meta-analyses
Base Line
BP mmHg
all cause mortality
RR (95%CI)
CV mortality
RR (95%CI)
MI
RR (95%CI)
Stroke
RR (95%CI)
ESRD
RR (95%CI)
>150 0.89 (0.8-0.99) 0.75 (0.36-0.87) 0.74 (0.63-0.87) 0.77 (0.65-0.91) 0.82 (0.71-0.94)
140-150 0.87 (0.78-0.98) 0.84 (0.76- 0.93)
<140 1.05 (0.95-1.16) 1.15 (1- 1.32)
BMJ 2016;352:i717 | doi: 10.1136/bmj.i717 42Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

43. Effect of antihypertensive
treatment at different blood
pressure levels in patients with
diabetes mellitus: systematic
review and meta-analyses
Results from meta-analyses
stratified according to
baseline systolic blood pressure
(SB P), reported for each
outcome separately
BMJ 2016;352:i717 | doi: 10.1136/bmj.i717
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44. 44
Aim: Control of BP among CKD and DM and Medication.
Hypertension Management and Cardiovascular risk Factors
Among Chronic Kidney Disease Patients with Diabetes
Jafar Al-Said, M.B. CHb. MD. FASN, FACP. Soni Murdeshwar. Bahrain Specialist Hospital
ESH Annual meeting 2014
Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

45. 45
Hypertension Management and Cardiovascular risk Factors
Among Chronic Kidney Disease Patients with Diabetes
Jafar Al-Said, M.B. CHb. MD. FASN, FACP. Soni Murdeshwar. Bahrain Specialist Hospital
ESH Annual meeting 2014
Matching:
CV risk profile:
Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

46. 46
Hypertension Management and Cardiovascular risk Factors
Among Chronic Kidney Disease Patients with Diabetes
Jafar Al-Said, M.B. CHb. MD. FASN, FACP. Soni Murdeshwar. Bahrain Specialist Hospital
ESH Annual meeting 2014
BP changes over follow up:
Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

47. 47
Number of AnitHTN. Medications:
Hypertension Management and Cardiovascular risk Factors Among
Chronic Kidney Disease Patients with Diabetes
Jafar Al-Said, M.B. CHb. MD. FASN, FACP. Soni Murdeshwar. Bahrain Specialist Hospital
ESH Annual meeting 2014
Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

48. 48
Hypertension Management and Cardiovascular risk Factors Among
Chronic Kidney Disease Patients with Diabetes
Jafar Al-Said, M.B. CHb. MD. FASN, FACP. Soni Murdeshwar. Bahrain Specialist Hospital
ESH Annual meeting 2014
Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

49. Control of Sugar in Diabetic Nephropathy
49Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

50. Increased incidence with eGFR < 60ml/min
Causes:
• Prolonged action of Insulin.
• Prolonged action of oral hypoglycemic agents.
• Chronic Malnutrition.
• Acute Calorie deprivation.
• Alcohol intake.
• Deficient Gluconeogenic precursor.
Hypoglycemic incidence in CKD
Tuttle K, Bakris G. et. al. Diabetic Kidney Disease: A Report From an ADA Consensus Conference. Diabetes
Care 2014;37:2864–2883 | DOI: 10.2337/dc14-1296 50Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

51. Decreased precision in CKD due to:
• Shorter RBC life span.
• Acid/Base.
• Anemia.
• Using Erythrocyte stimulating factors.
HbA1C in CKD
Vos FE, Schollum JB, Coulter CV, Doyle TCA, Duffull SB, Walker RJ. Red blood cell survival in long-term dialysis patients.
Am J Kidney Dis 2011;58:591–598.
Nakao T, Matsumoto H, Okada T, et al. Influence of erythropoietin treatment on hemoglobin A1c levels in patients with
chronic renal failure on hemodialysis. Intern Med 1998;37:826–830
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52. Optimal survival with
HbA1C for ESRD 7-8%.
U curve of HbA1C.
Shurraw S, Hemmelgarn B, Lin M, et al.; Alberta Kidney
Disease Network. Association between glycemic control and
adverse outcomes in people with diabetes mellitus and
chronic kidney disease: a population-based cohort study.
Arch Intern Med 2011;171:1920–1927
Kalantar-Zadeh K. A critical evaluation of glycated protein
parameters in advanced nephropathy:a matter of life or
death: A1C remains the gold standard outcome predictor in
diabetic dialysis patients. Diabetes Care 2012;
35:1625–1628.
Ramirez SPB, McCullough KP, Thumma JR, et al. Hemoglobin
A(1c) levels and mortality in the diabetic hemodialysis
population: findings from the Dialysis Outcomes and Practice
Patterns Study (DOPPS). Diabetes Care 2012;35: 2527–2532
52Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

53. • HbA1C.
• Fructosamine.
• 1,5 anhydroglucitol.
• Glycated Albumin.
Glycemic markers
Kim WJ, Park C-Y, Lee K-B, et al. Serum 1,5-anhydroglucitol concentrations are a reliable index of glycemic control in type 2 diabetes with
mild or moderate renal dysfunction. Diabetes Care 2012;35:281–286.
Inaba M, Okuno S, Kumeda Y, et al.; Osaka CKD Expert Research Group. Glycated albumin is a better glycemic indicator than glycated
hemoglobin values in hemodialysis patients with diabetes: effect of anemia and erythropoietin
injection. J Am Soc Nephrol 2007;18:896–903
53Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

54. Metformin Dose adjustment according to eGFR
Tuttle K., Bakris G. et.al Diabetic Kidney Disease: A report from an ADA Consensus. Diabetes Care.
2014;37:2864–2883 | DOI: 10.2337/dc14-1296
54Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

55. Dose adjustment for Oral Hypoglycemic agents
Tuttle K, Bakris G. et. al. Diabetic Kidney Disease: A Report From an ADA Consensus Conference. Diabetes Care 2014;37:2864–2883 DOI:
10.2337/dc14-1296
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56. • CKD I – IV SAME AS GENERAL POPULATION.
<100mg/dl for LDL / 30-40% reduction from baseline.
• ESRD. benefit is not confirmed with lipid lowering.
• Statins recommended for all diabetic CKD not on dialysis.
Hyperlipidemia in CKD
Palmer SC, Craig JC, Navaneethan SD, Tonelli M, Pellegrini F, Strippoli GFM. Benefits and harms of statin therapy for persons with chronic kidney disease:
a systematic review and meta-analysis. Ann Intern Med 2012;157:263–275.
Haynes R, Lewis D, Emberson J, et al. Effects of lowering LDL cholesterol on progression of kidney disease. J Am Soc Nephrol. 8 May 2014
Wanner C, Tonelli M, Cass A, et al. KDIGOclinical practice guideline for lipid management in CKD: summary of recommendation statementsand
clinical approach to the patient. Kidney Int2014;85:130321309Reference 34
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57. Incidence 15-25%.
Causes:
• Steroid.
• Calcineurin inh. (Tacrolimus).
• Increased Appetite.
• Wt. Gain.
Outcome:
Increased CV risk.
Reduce graft survival.
New Onset Post Transplant Diabetes
Sarno G, Mehta RJ, Guardado-Mendoza R,Jimenez-Ceja LM, De Rosa P, Muscogiuri G. New-onset diabetes mellitus: predictive
factors and impact on the outcome of patients undergoing liver transplantation. Curr Diabetes Rev 2013;9:78–85.
Chakkera HA, Mandarino LJ. Calcineurin inhibition and new-onset diabetes mellitus after
transplantation. Transplantation 2013;95:647–652. 57Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

58. Management outcome of Chronic Kidney
Disease in our Nephrology OPD
JAFAR AL-SAID, TEERATH KUMAR, SONI MERDASHWAR
BAHRAIN SPECIALIST HOSPITAL
58
• HTN and CV highlight Dec. 2012
• ESH annual Meeting 2013
Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

59. Aim of the Study
• What are the CV risk factors in CKD patients followed in our
clinic?
• What is the rate of progression of their kidney function?
• What are the factors related to the final kidney function?
59Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

60. Methodology
Retrospective Observational.
CKD patient followed in Nephrology OPD over 8.5 years (102month) from Oct.
2003 till April 2012.
Exclusion:
1. Patient with only one visit.
2. No lab workup.
3. Primary Glomerulonephritis.
4. Transplant.
5. Pregnant.
Inclusion:
1. Adult > 14 years.
2. Had CKD.
3. Followed in OPD.
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61. Results
• N = 245 patients.
• Mean follow up: 23.6 month (SE 1.6).
• Mean Age: 58.7 years (SE 0.9).
• Mean BMI: 30.9kg/m2 (SE 0.7)(SD10.5)
• Males: 60.8%
61Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

62. Cardiovascular risk factors
Total CKD population, n = 245
91%
72%
60%
43%
20%
9%
6%
0%
20%
40%
60%
80%
100%
HTN Hyperlipi. DM Hyperuric. IHD PVD Stroke
Type of CV disease
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63. Demographics of
into DM and Non DM
DM Non DM
P
N 147 98
Age 61.8(0.9) 54(1.8) <0.0001
Male gender 55% 69% 0.047
BMI 31.6(0.6) 30(1.4) 0.2
63Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

64. Dividing the total population
into DM and Non DM
DM Non DM p
Mean of first eGFR (SE) 42.8 (1.8) 49.4(2.1) 0.02
Mean of Last eGFR (SE) 41(2.1) 51.2(3) 0.005
p 0.58 0.22
Difference in eGFR -0.9(1.7) -2.4(2) 0.5
64Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

65. Variables Correlation Coefficient p
Systolic1 -0.2 0.012
Hb1 0.36 0.001
Alb1 0.25 0.03
Follow up duration 0.23 0.008
Systolic2 -0.19 0.03
Hb2 0.4 0.001
Alb2 0.27 0.025
PO4 2 -0.4 0.004
Beta blocker -0.19 0.025
Ca-block -0.22 0.012
Vasodilator -0.23 0.007
NTG -0.26 0.002
Correlation of the last eGFR with demographic factors, CV risk factors and
the medications used in DM
65Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

66. S.Cr and eGFR changes over follow up
in HTN and DM subgroups
Non HTN &
Non DM (SE)
Non HTN
& DM (SE)
HTN &
Non DM (SE)
HTN &
DM (SE)
P
First Cr 1.4 (0.1) 1.8 (0.34) 1.8 (0.1) 1.9 (0.08) <0.001
Last Cr 1.3 (0.09) 1.8 (0.5) 1.9 (0.14) 2.3 (0.16) 0.5
p 0.07 0.75 0.35
First eGFR 58.7 (4.2) 52.8 (10.7) 47.8 (2.7) 42.2 (1.8) 0.3
Last eGFR 59.2 (4.6) 61.7 (13.5) 49.9 (3.7) 39.6 (2.1) 0.1
P 0.18 0.13 0.3 0.8
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67. 87%
55%
0%
20%
40%
60%
80%
100%
HTN DM
ESRD with HD at Bahrain specialist Hospital
N = 118 patients
67Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016

68. • Diabetic Nephropathy occur in 20-40% of patients with Dm.
• Its manifestation require Genetic, Hemodynamic and Metabolic
factors.
• Growth factors and cytokines play major role in its development.
• Proteinuria, decreased GFR and HTN are its main clinical features.
• ESRD could develop in 40-80%.
• Management require tight control of BP, sugar and lipids.
Conclusion
68Jafar Al-Said. GCC Diabetes Conference Bahrain March 2016