This document discusses chronic kidney disease (CKD) and its management. It provides definitions of CKD and outlines its stages according to the KDIGO classification system. Diabetes and hypertension are highlighted as leading causes of CKD globally. Early detection of CKD is important as it can be asymptomatic for long periods. Screening high-risk individuals through estimated GFR and urine albumin or protein tests is recommended. Left unmanaged, CKD can progress to end-stage renal disease requiring renal replacement therapies like dialysis, which are costly treatments.

1. OUTPATIENT MANAGEMENT
OF CKD PATIENTS
DR SANJAY MAITRA
MD,DM(PGI,CHD),CLIN.FELLOWSHIP TORONTO UNIV.
SR.CONSULTANT NEPHROLOGIST,APOLLO HEALTH CITY,
HYDERABAD

5. WHAT IS WORLD KIDNEY DAY?
• World Kidney Day (WKD) is a global health awareness
campaign focusing on the importance of the kidneys and
reducing the frequency and impact of kidney disease and
its associated health problems worldwide.
• World Kidney Day is observed annually on the 2nd
Thursday in March
• World Kidney day is a joint initiative of the (ISN) and
the International Federation of Kidney Foundations(IFKF).

6. WORLD KIDNEY DAY –FOCUS AREAS
 2016 Kidney disease and children
 2015 Kidney Health for All
 2014 Chronic Kidney Disease (CKD) and aging
 2013 Kidneys for Life – Stop Kidney Attack!
 2012 Donate – Kidneys for Life – Receive
 2011 Protect your kidneys: Save your heart
 2010 Protect your kidneys: Control diabetes
 2009 Protect your kidneys: Keep your pressure down
 2008 Your amazing kidneys!
 2007 CKD: Common, harmful and treatable
 2006 Are your kidneys OK?

7. WHAT IS CKD- CURRENT
UNDERSTANDING
Heterogeneous group of disorders
characterized by alterations in kidney
structure and function, which manifest in
various ways depending upon the underlying
cause or causes and the severity of disease

8. WHAT IS CKD- CURRENT UNDERSTANDING
Structural or functional abnormalities of the kidneys for ≥3 months as
manifested by
Kidney damage with or without decreased GFR ,as defined by
1.)Pathologic abnormalities
Markers of Kidney damage like
Urinary abnormalities(proteinuria)
Blood abnormalities (renal tubular syndromes)
Imaging abnormalities
Kidney transplantation
2.)GFR < 60ml/min/1.73m2 ,with or without kidney damage
CKD – Chronic Kidney Disease, GFR- Glomerular Filtration Rate

9. CKD- a continuum
Stages of CKD –KDIGO 2012

10.  Chronic kidney disease is an increasing public health issue.
 Prevalence is estimated to be 8–16% worldwide.
 Complications include increased all-cause and cardiovascular
mortality
 kidney-disease progression, acute kidney injury,
 Cognitive decline, anaemia, mineral and bone disorders, and
fractures.

11. CHRONIC KIDNEY DISEASE –GLOBAL
DIMENSIONS AND PERSPECTIVES
Worldwide, diabetes mellitus is the most common cause of chronic
kidney disease
In some regions of the world herbal and environmental toxins, are more
common
 The poorest populations are at the highest risk
 Screening and intervention can prevent chronic kidney disease
Wherever management strategies have been implemented the incidence
of end-stage kidney disease has been reduced
 Awareness of the disorder, however, remains low in many communities
and among many physicians.

12. USRDS ADR, 2007
Diabetes and hypertension are
leading causes of kidney failure
Incident ESRD rates, by primary diagnosis, adjusted for age, gender, & race.

13.  It is estimated that over 40% of all deaths in India are due to
NCD.
 The exact burden of chronic kidney disease or ESRD is not
known.
 CKD incidence is estimated at 800pmp
 ESRD incidence at 152 per million population.
 Diabetic kidney disease is the commonest cause of ESRD in

14. CURRENT STATUS OF END-STAGE RENAL
DISEASE CARE IN INDIA
CKD of undertermined etiology forms a large proportion as
well.
 Environmental factors have been postulated in its causation.
Economic issues limit the availability of renal replacement
therapy to large sections of the population.
 Hemodialysis and peritoneal dialysis are equally expensive.
Dialysis prescriptions are not optimized.
 Renal transplant is the most suitable option for a majority of
patients
Increasing public awareness and educating physicians to

15. Cross sectional study involving 52,273 patients
Mean age 50.1±14.6 yrs
M:F ratio 70:30
Diabetic nephropathy –commonest cause of CKD (31%)
CKD of unknown aetiology (16%)
CGN (14%)
Hypertensive nephrosclerosis (13%)

16. Diabetics likely to be detected early
Patients of unknown etiology are likely to be younger ,females and to have CKD-5
INDIAN CKD REGISTRY DATA-2012

17. • Family history of polycystic kidney
disease or other genetic kidney
disease
• Renal dysplasia or hypoplasia
• Urologic disorders—especially
obstructive uropathies
Hogg, et al., 2003
CKD is less common in children but
there are risk factors

18. 2 SIMPLE TESTS WILL IDENTIFY CKD IN ADULTS
• eGFR - Estimated GFR from serum creatinine using the MDRD
equation
• UACR - Urine albumin to creatinine ratio on a “spot” urine
sample
• 24-hour urine collections are NOT needed
- Diabetics should be tested once a year. Others at risk can be tested less
frequently as long as normal.

19. • MDRD estimating equation is not applicable
to children
• Updated Schwartz formula provides
reasonable estimate in children with mild-
moderate CKD
(GFR – 15-75 mL/min/1.73 m2)
Updated Schwartz Formula
eGFR = k * Ht/Scr
Where k=0.4, Ht in cm and Scr in mg/dL and measured by
enzymatic methodology
ESTIMATION OF GFR IN CHILDREN

20. USRDS ADR, 2006
CKD IS DISPROPORTIONATELY COSTLY
Distribution of costs for CKD, HTN, & diabetic patients in Medicare population, 2004.

21. Monthly Cost Of haemodialysis at 3 HD/wk Rs 12,000- Rs 30,000
Monthly cost Of Erythropoeitin per month Rs 7,000-Rs 10,000
Monthly cost of CAPD 3 exchanges per
day
Rs. 20,000-Rs 25,000
Cost of transplant procedure Rs 3,00,000- Rs, 7,00,000
Cost of immunosuppressive medicines
(Using Tacrolimus,MMF and steroids)
Rs 10,000-Rs 15,000 per
month
Approx.cost of Renal replacement therapy in
India

23. TYPICAL PROGRESSION OF DIABETIC KIDNEY
DISEASE
Exposure to diabetes is
required for diabetic
nephropathy to develop in
susceptible patients.
The time at which the
complication becomes clinically
apparent and the rate at which
it progresses is variable and
can be modified by careful
management of glycemia,
hypertension, and glomerular
hypertension.
ESRD, End-stage kidney
23
Seaquist ER, Ibrahim HN. J Clin Endocrinol Metab. 2010 Jul;95(7):3103-10
Risk of developing Diabetic Nephropathy equal in Type 1 & Type 2
Diabetes

25. CHANGING PRESENTATION OF DIABETIC
NEPHROPATHYIn Type 1 Diabetes –
• Longitudinal studies show that 40% develop persistent proteinuria at 15 yrs
and maximal proteinuria by 25yrs
• Currently there is decrease in proteinuria and postponement of time to ESRD
• Due to better glycaemic control,BP control,RAAS blockade and lipid management
• ESRD postponed but not stopped.
Contrary to conventional teaching a significant number of patients present
with only e-GFR decline and no or minimal proteinuria, particularly the
elderly
• Previous data showed 85-100 % microalbuminuric patients progressed to
macroalbuminuria
• Recent data shows by 2-3 yrs most will revert to normal albumin excretion
• Lower levels of microalbuminuria cannot be considered as established diabetic
nephropathy

26. CHANGING PRESENTATION OF DIABETIC
NEPHROPATHY

27. CHANGING PRESENTATION OF
DIABETIC NEPHROPATHY
In Type 2 Diabetics
• the incidence of DKD has not come down
• Many patients of Type 2 DM and 5-30 % of Type 1 DM with CKD have
normal urinary protein excretion, which does not progress
• Improved cardiac survival have increased the chances of DKD
In Type 2 Diabetes patients with indications for biopsy
• 1/3 had classical diabetic changes
• 1/3 had interstitial disease ,tubular atrophy , hypertensive changes
• 1/3 had mixed changes

28. TYPE 2 DIABETES IN YOUNG AND THE
ELDERLY• Diabetic Kidney Disease is more common in young
• Recent Canadian study showed 27% of youth had
microalbuminuria and 4.7% had macro-albuminuria after
1.6yrs of diagnosis
• Young Type 2 diabetics were 4 times more likely to develop
kidney failure than Type 1 diabetics
• They have more risk factors like obesity, insulin resistance,
hypertension and dyslipidemia
• CKD is also more prevalent in elderly , obese , certain ethnic
groups and the disadvantaged populations

29. DIABETES-RELATED COMPLICATIONS IN US
1990–2010
N Engl J Med 2014;370:1514-23

30. BUT FEW ARE AWARE OF IT – EVEN THOSE
WITH EGFR LESS THAN 30
0
10
20
30
40
50
60
eGFR of 30-59 eGFR of 15-29
PercentReportBeingAwareof
HavingWeakofFailingKidneys
Men
Women
Coresh, et al., 2007

31. CKD IS PREVALENT IN CVD
Ix, et al., 2003; Anavekar, et al., 2004; Shlipak, et al., 2004.
0
20
40
60
CAD
CrCl ≤60 mL/min
AMI
GFR <60 mL/min
CHF
GFR ≤60 mL/min
23%
46%
33%
PatientsWithCKD(%)

32. IN ADDITION TO ESRD, CKD LEADS
TO CVD
Go, et al., 2004
1.0
2.8
3.4
2.0
1.4
0.0
0.5
1.0
1.5
2.0
2.5
3.0
3.5
4.0
≥ 60 45-59 30-44 15-29 < 15
AdjustedHazardRatio
eGFR
Adjusted* hazard ratio for CVD events

33. YOUNGER PEOPLE WITH CKD ARE MORE LIKELY TO DEVELOP ESRD BEFORE
DEATH
Copyright ©2007 American Society of Nephrology
O'Hare, 2006
Annual mortality by age group and eGFR.

34. Diabetes: A global emergency
Diabetes is likely the 5th leading cause of death worldwide

35. 2014 2035
WORLD
387
million
WORLD
592
million
people living
with diabetes
Middle East and North Africa 85%
South East Asia 64%
South and Central America 55%
Western Pacific 46%
North America and Caribbean 30%
Europe 33%
Africa 93%
53%

36. WHO ARE THE PATIENTS AT INCREASED
RISK OF CKD?
• Diabetes
• Hypertension
• Autoimmune diseases
• Systemic infections
• UTI, nephrolithiasis, lower urinary-tract obstruction
• Hyperuricemia
• Acute kidney injury
• Family history of chronic kidney disease
• Sociodemographic risk factors
• Older age
• Black race
• Smoking
• Heavy alcohol use
• Obesity
• NSAIDs

37. SHOULD CLINICIANS SCREEN PATIENTS
FOR CKD? IF SO, HOW?
Screen individuals at increased risk for CKD
Those older than 55 years
Those with hypertension, diabetes, or obesity
Screening: estimate GFR and test for kidney damage markers
Serum creatinine to estimate GFR
Urinalysis for leukocytes and red blood cells
Qualitative test for urine albumin (or protein) with dipstick; if positive, measure
amount to calculate an albumin-to-creatinine (or a protein-to-creatinine) ratio

38. URINE ALBUMIN & PROTEIN TO
CREATININE RATIO
• Albumin-to-creatinine ratio
• Normal to mildly increased <30 mg/g
• Moderately increased 30-300 mg/g
• Severely increased >300 mg/g
• Protein-to-creatinine ratio
• Normal to mildly increased <150 mg/g
• Moderately increased 150-500 mg/g
Severely increased >500 mg/g
Type 2 diabetes: screen for albuminuria annually
Positive when >30 mg/g creatinine in a spot urine sample

39. 24-yo
Black Man
63-yo
White Man
59-yo
White Woman
SCr 1.3 mg/dL 1.3 mg/dL 1.3 mg/dL
GFR as
estimated
by MDRD
Study
equation
≥60
mL/min/1.73 m2
45
mL/min/1.73 m2
59
mL/min/1.73 m2
THE PERILS OF USING SERUM
CREATININE TO “GUESS”
LEVEL OF RENAL FUNCTION

40. CKD IS STILL NOT BEING IDENTIFIED
• Estimated GFR reporting is not
universal
• Only 38% of labs routinely report
eGFR with creatinine
• CKD is usually not coded as a diagnosis
• Less than 40% of patients with eGFR
<30 were coded
Stevens, et al., 2005; NKDEP, 2008

41. ARE PREVENTIVE MEASURES USEFUL FOR
PATIENTS AT INCREASED RISK FOR CKD?
• Diabetes
• Hyperglycemia is associated with development and progression of diabetic nephropathy
• Good glycemic control reduces CKD risk
• Maintain hemoglobin A1c ~7% with dietary interventions, oral hypoglycemic medications, and
insulin
Hypertension
Hastens renal function decline
Treatment reduces CV risks but not CKD risk
Maintain blood pressure <140/90 mm Hg with lifestyle modification and antihypertensive drug
therapy

42. CLINICAL BOTTOM LINE: SCREENING AND
PREVENTION...
 Who to screen
 Individuals > 55 years of age
 Individuals with hypertension or diabetes
 How to screen
 Estimate GFR from serum creatinine, and do a urinalysis
 In patients with diabetes
• Screen for proteinuria with urine albumin-to-creatinine or protein-to-creatinine
ratio
• Maintain strict glycemic control to prevent CKD

43. WHAT CLINICAL MANIFESTATIONS
SHOULD CLINICIANS LOOK FOR WHEN
EVALUATING PATIENTS FOR CKD?
 Findings associated with diabetes and hypertension
 History of HF or cirrhosis suggests decreased renal perfusion
 Infection with HBV, HCV, or HIV may cause proteinuria
 Family history of kidney disease suggests polycystic disease,
the Alport syndrome, or medullary cystic kidney disease
 Urinary problems may reflect underlying urinary tract disease
 Skin rash, arthritis, mononeuropathy, or systemic symptoms
suggests vasculitis, including lupus
 Recent diarrhea, bleeding, or dehydration may decrease renal
perfusion that leads to acute kidney injury
 A medication history may reveal a drug cause of CKD

44. PHYSICAL EXAMINATION
• Check for orthostasis
• Look for rashes and petechiae
• Examine the fundus for diabetic retinopathy or
hypertensive retinopathy
• Evaluate for heart failure
• A renal bruit suggests renal artery stenosis
• Inflamed joints suggest vasculitis or autoimmune
processes
• Asterixis or encephalopathy suggests uremia

45. • Serum creatinine (to estimate GFR)
• Serum electrolytes
• CBC and lipid profile
• Urinalysis (specific gravity, pH, red cells, leukocytes)
• If GFR <60 mL/min per 1.73 m2
• Serum calcium, phosphorus, parathyroid hormone, albumin
WHAT LABORATORY TESTS AND
IMAGING SHOULD CLINICIANS USE
TO EVALUATE CKD?
 Renal ultrasound
 For hydronephrosis, cysts, and stones
 To assess echogenicity, size, kidney symmetry

46. HOW SHOULD CLINICIANS CLASSIFY
CKD AND CONSTRUCT A
DIFFERENTIAL DIAGNOSIS?
• By GFR and albuminuria
• Determine cause based on:
• Presence or absence of systemic disease
• Presumed location of damage in the kidney (glomerular,
tubulointerstitial, vascular, or cystic)
 Classify patients with CKD into 1 of 3 broad categories:
 Diabetic kidney disease
 Hypertensive kidney disease
 Non-hypertensive, non-diabetic kidney disease

47. • Persistent albumin-to-creatinine ratio ≥300mg/g
• Nephritic syndrome (hematuria, proteinuria, and
hypertension)
• Sustained hematuria (red cell casts or RBC > 20/high
power field)
• No clear etiology of CKD
• Type 2 diabetes with proteinuria w/o coexistent
retinopathy or neuropathy
• Rapid decline in kidney function (>5 mL/min per 1.73 m2
per year)
WHEN SHOULD CLINICIANS
CONSIDER CONSULTING WITH A
NEPHROLOGIST FOR DIAGNOSING
PATIENTS WITH POSSIBLE CKD?

48. CLINICAL BOTTOM LINE: DIAGNOSIS...
 CKD is defined as kidney damage or a GFR <60 mL/min per
1.73 m2 for > 3 months
 Classify
 Diabetic nephropathy
 Hypertensive nephropathy
 Nondiabetic, nonhypertensive kidney disease
 Then, into groups based on levels of GFR and albuminuria
 History and physical exam often point to a cause
 Definitive diagnosis requires:
 Diagnostic tests
 Renal ultrasound
 Sometimes renal biopsy

49. EARLY TREATMENT CAN MAKE A
DIFFERENCE
100
10
0
No Treatment
Current Treatment
Early Treatment
4 7 9 11
Time (years)
Kidney Failure
GFR(mL/min/1.732)

50. WHAT CAN PRIMARY CARE PROVIDERS DO?
• Recognize and test at-risk patients
• Educate patients about CKD and treatment
• Focus on good glycemic control in people with diabetes
• For those with CKD:
• Blood pressure below 130/80
• Use an ACE inhibitor or ARB
• More than one drug is usually required
• A diuretic should be part of the regimen

51. WHAT NON-DRUG THERAPIES
SHOULD CLINICIANS RECOMMEND?
• Quit smoking, and exercise 30 min/d on most
days
• Limit alcohol intake
• Maintain BMI within normal range
• Eat a diet high in fruits, vegetables, and whole
grains
• DASH diet recommended if GFR >60 mL/min per
1.73 m2 and high normal blood pressure or stage
1 hypertension
• If hypertension present: restrict salt intake <2.0
g/d

52. WHICH DRUGS AND OTHER AGENTS CAUSE
ACUTE KIDNEY INJURY IN PATIENTS WITH CKD?
• Nephrotoxic medications
• Aminoglycoside antibiotics, amphotericin B, NSAIDS,
radiocontrast agents
• If radiocontrast agents essential: give sodium bicarbonate or
0.9% normal saline IV before and after procedure for
patients at increased risk for contrast nephropathy
• Consider N-acetylcysteine before and after radiocontrast
only in high-risk patients
• Avoid high doses of gadolinium contrast in stages 4 and 5
due to risk for nephrogenic systemic fibrosis
• Adjust dosing of other medications to avoid other AEs

53. WHAT IS THE ROLE OF BLOOD
PRESSURE MANAGEMENT?
• To reduce CVD risk, treat to <140/90 mm Hg
• If proteinuria is significant or urine albumin-to-creatinine
ratio >30mg/g: treat to <130/80 mm Hg
• Use ACE inhibitors and ARBs (improve kidney outcomes)
 Combination therapy often needed
 Diuretics reduce extracellular fluid volume, lower BP, and
reduce risk for CVD
 Diuretics also potentiate effects of antihypertensives
 Thiazide-type diuretic if GFR ≥30 mL/min per 1.73 m2
 Loop diuretic if GFR <30 mL/min per 1.73 m2

54. WHEN SHOULD CLINICIANS
PRESCRIBE ACE INHIBITORS VERSUS
ARBS?
• Prescribe either for reducing progression of diabetic
nephropathy
• Prescribe either in hypertension or in diabetes when
urine albumin excretion >30mg / 24h
• Prescribe either in non-diabetic proteinuria
• Do not combine an ACE inhibitor with an ARB
• Monitor patients closely for side effects and adjust dose
as needed
• Safe to continue medication if GFR declines < 30% over
4 mos and serum potassium <5.5 mEq/L

55. WHAT IS THE ROLE OF GLYCEMIC
CONTROL IN PATIENTS WITH
DIABETES AND CKD?
• Good glycemic control reduces:
• Progression of CKD
• Incidence proteinuria
• Maybe end-stage renal disease
• However, CKD increases risk for hypoglycemia
• Current CKD guidelines recommend a goal A1c level
~7%
• Avoid using metformin if GFR <30 mL/min per 1.73
m2

56. HOW SHOULD CLINICIANS MANAGE
METABOLIC COMPLICATIONS?
• Vitamin D and phosphorous metabolism
• Derangements occur if GFR <30-40 mL/min per 1.73 m2
• Use dietary phosphorous restriction, phosphate binders, and vitamin D
supplementation
 Hyperkalemia
 Dangerous elevations occur mostly only in stages 4 / 5
 Use dietary potassium restriction, and if necessary, sodium
polystyrene sulfonate
 Hyperkalemia >6mEq/L or hyperkalemic EKG change
requires emergency treatment with IV calcium gluconate,
glucose, insulin, bicarbonate (if acidosis present), and
sodium polystyrene sulfonate
 If these measure fail, hemodialysis may be needed

57. • Metabolic acidosis
• Seldom significant until GFR <30 mL/min per 1.73 m2
• Contributes to CKD progression, insulin resistance,
decreased cardiorespiratory fitness, altered bone
metabolism
• Use alkali therapy with serum bicarbonate <22 mmol/L to
maintain serum bicarbonate levels within normal range

58. HOW SHOULD CLINICIANS MANAGE
PATIENTS WITH ANEMIA?
• Measure hemoglobin and hematocrit, RBC indices,
reticulocyte count, serum iron, percent transferrin
saturation, vitamin B12 and folate levels, serum ferritin
• Identify potential sources of bleeding
• Treat with erythropoietin when hemoglobin drops below
9-10 g/dL
• Prescribe oral / IV iron as needed to maintain iron stores
• Maintain hemoglobin levels <11.5 g/dL
• Use caution with active malignancy or history of stroke

59. HOW SHOULD CLINICIANS TREAT
CARDIOVASCULAR RISK FACTORS?
• Aggressively reduce risk factors for atherosclerosis
• Encourage a healthy lifestyle regarding smoking,
exercise, alcohol intake, and BMI
• Assess for other cardiovascular risk factors
• Check BP, and treat hypertension
• Screen for diabetes, and treat elevated blood glucose
• For people with CKD, ACC/AHA guidelines recommend
treatment with statin or statin/ezetimibe combination
regardless of cholesterol level

60. HOW SHOULD CLINICIANS
MONITOR PATIENTS WITH CKD?
• Once a year check BP; GFR; hemoglobin level; and
serum potassium, calcium, phosphorous, PTH, and
albumin More frequent monitoring may be needed if
 CKD is moderate to severe
 History of rapid decline in kidney function
 There are risk factors for faster progression (smoking,
poorly controlled hypertension or diabetes, proteinuria)
 Exposure to a cause of acute kidney injury
 Active or changing therapeutic interventions to treat CKD,
hypertension, or proteinuria

61. WHAT ARE THE INDICATIONS FOR
RENAL REPLACEMENT THERAPY?
• Volume overload unresponsive to diuretics
• Pericarditis
• Uremic encephalopathy
• Major bleeding secondary to uremic platelets
• Hypertension that does not respond to treatment
• Hyperkalemia and metabolic acidosis that cannot be
managed medically
• Progressive “uremic” symptoms, which include fatigue;
anorexia, nausea or vomiting; malnutrition; and insomnia

62. WHEN SHOULD CLINICIANS CONSIDER
CONSULTING A NEPHROLOGIST FOR
TREATING PATIENTS WITH CKD?
• To manage complications of advanced CKD
• For assistance with a care plan for advanced or complex
renal disease
• For therapeutic decision-making about complex acute or
chronic glomerular and tubulointerstitial diseases
• When dialysis is anticipated
• When GFR first falls below 30 mL/min per 1.73 m2
• To discuss treatment for end-stage renal disease
• For counseling, psychoeducational interventions, and
referral for fistula placement

63. CLINICAL BOTTOM LINE:
TREATMENT...
 The goals are to slow progression of CKD and prevent
complications from cardiovascular disease
 Maintain normal blood pressure in patients with
hypertension
 Include an ACE inhibitor or an ARB when treating
hypertension
 Control glycemia in patients with diabetes
 Manage electrolyte disturbances, anemia, secondary
hyperparathyroidism, and malnutrition
 Refer to a nephrologist as CKD progresses

64. PRIMARY CARE PROVIDERS –
FIRST LINE OF DEFENSE AGAINST CKD
• Primary care professionals can play a significant
role in early diagnosis, treatment, and patient
education
• Therapeutic interventions for diabetic CKD are
similar to those required for optimal diabetes care
• Control of glucose, blood pressure, and
lipids
• A greater emphasis on detecting CKD, and
managing it prior to referral, can improve patient
outcomes
CKD is Part of Primary Care