Renal Failure
in the Primary Care setting
1
Hasan Ismail
PGY III – Family Medicine
Lebanese University
Objectives
• To identify the role of the Family Physician in
the management of CKD
• To be aware of referral indications
• To be able to treat and follow most of the CKD
complications
2
• A 46-year-old woman - First visit
• CC :Decreased urinary output for 5 months with
a foamy appearance.
• Swelling in both legs
• non bloody, non bilious emesis a few times a
week.
3
Case scenario 1
• Diet: “I eat the best I can for what I afford but
often have very little appetite”
4
• Diabetes since 10 years ago and has been taking
insulin for 2 years.
• She does not check her sugars at home because
she does not like to "stick" herself.
• Obese
• Her temperature is 37.2°C, her heart rate is
• 108 beats/min, her blood pressure is 198/105 mm
Hg, her respiration is 19 breaths/
• min, and her oxygen saturation is 94% on room air.
• (HEENT) examination reveals periorbital edema.
• Her skin is hyperpigmented on both lower
extremities.
5
• Tachycardia with an S1, S2, S4 gallop, Vesicular
breath
• No jugular venous distension and no carotid
bruits.
• Abdomen is nontender, with no bruits or
masses palpated.
• The lower extremities reveal pitting pretibial
edema with a pit recovery time less than 40
seconds.
6
Labs
• Urinalysis
 Hyaline casts
 3+ proteinuria
 Glucose
 negative for ketones.
• Her hemoglobin is 10.9 g/dl and her hematocrit is
32% with a mean corpuscular volume (MCV) of
82.3 g/dl.
7
Case 1 Summary
• This is a 46-year-old woman with chronic kidney
disease (CKD). She has a history of uncontrolled
diabetes and currently has uncontrolled
hypertension.
• She presents with periorbital edema, long-
standing lower-extremity edema, an S4 and
central obesity.
• The urinalysis shows hyaline casts,
• 3+ proteinuria and glucose, negative ketones, and
hemoglobin 10.9 g/dL with an MCV of82.3 g/dL.
8
What is your next
diagnostic step?
9
• serum electrolytes
• blood urea nitrogen (BUN)
• Creatinine
• imaging of the kidneys
10
Next step in therapy ?
11
• Further history to identify and remove any
offending agents (such as nonsteroidal anti-
inflammatory drugs [NSAIDs])
• Control of blood pressure and diabetes
• May require dialysis if she develops
complications such as pulmonary edema,
severe hyperkalemia, or anuria
12
• A significant reduction in urine output requires
immediate evaluation of creatinine function and
volume status.
• Volume status is assessed by skin turgor, mucous
membranes, specific gravity in the urinalysis,
and orthostatic blood pressure.
• A low volume status with an elevated creatinine
requires that the patient be given IV fluids to see
if there can be any recovery of kidney function.
13
• The patient's uncontrolled diabetes and
hypertension predispose her to kidney
damage.
• Another common offender is a patient with
this history who is taking NSAIDs.
• This will increase the patient's already high
risk of damage.
14
Etiologies
• DM, HTN, and glomerulonephritis.
• Diabetic kidney disease occurs in 30% to 40% of
type I DM, in 25% of type II DM, and in 24% of
HTN patients.
• 20% to 60% of DM patient are HTN !
•  Many patients present at a later stage of CKD
and it is then difficult to determine the etiology 15
16
Davidson’s Principles and practice of medicine, 23rd edition
• Progressive destruction of nephrons;
• GFR will drop gradually, and plasma Cr
values will approximately double, with
50% reduction in GFR and 75% loss of
functioning nephrons mass.
• Hyperkalemia usually develops when
GFR falls to <20 to 25 mL/min
17
18
Screening
Recommendations ?
• USPSTF 2012
- Insufficient evidence to recommend for or against
routine screening.
• ACP 2013, AAFP 2014
- Do not screen adults unless they have symptoms
or risk factors.
- Adults taking an ACE inhibitor or ARB should not
be tested for proteinuria, regardless of diabetes
status.
19
* USPSTF. Chronic Kidney Disease (CKD): Screening. 2012.
** AAFP Clinical Recommendations: Chronic Kidney Disease. 2014.
Ann Intern Med. 2013;159(12):835
• NICE 2014
- Monitor glomerular filtration rate (GFR) at least
annually in people prescribed drugs known to be
nephrotoxic (calcineurin inhibitors, lithium, or
nonsteroidal anti-inflammatory drugs (NSAIDs)..)
- Screen renal function in people at risk for CKD
(DM, HTN, CVD, structural renal disease,
nephrolithiasis, BPH, multisystem diseases with
potential kidney involvement, stage 5 CKD or
hereditary kidney disease, or personal history of
hematuria or proteinuria
20Early identification and management of chronic kidney disease in adults in primary and secondary care. London (UK):
NICE; 2014
HOW TO SCREEN ?
21
22
serum creatinine
Estimation of GFR
Urine albumin/ creatinine ratio
Urinalysis
Definition
≥3 mo w/ GFR <60 mL/min/1.73 m2
or
signs of kidney damage:
Proteinuria/albuminuria, pathology on renal
biopsy/imaging
23
Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice
guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013; 3(1): 1-150.
24
(Kid Int 2013;3:19)
CKD Staging
Albuminuria Stage
25
based on albuminuria (mg/d) or
spot urine Alb/Cr (mg) ratio (ACR):
• A1: nl or mildly ↑ (ACR <30)
• A2: mod ↑ [formerly microalbuminuria]
(ACR 30–299)
• A3: or severely ↑ [formerly macroalbinuria]
(ACR ≥300)
(Kid Int 2013;3:19)
Geriatric Considerations
• GFR normally decreases with age, despite
normal creatinine (Cr).
• Adjust renally cleared drugs for GFR in the
elderly.
26
Pediatric Considerations
• CKD definition is not applicable for children <2
years because of lower GFR even when
corrected for body surface area.
• Calculated GFR based on serum Cr is used in
this age group.
27
Pregnancy Considerations
• Renal function in CKD may deteriorate during
pregnancy.
• Cr >1.5 and hypertension (HTN) are major risk
factors for worsening renal function.
• Increased risk of premature labor, preeclampsia,
and/or fetal loss
• ACE inhibitors and angiotensin receptor blockers
(ARBs) are contraindicated due to teratogenicity.
• Use diuretics with caution
28
Assessment : History taking
Patients with CKD stages 1 to 3 are usually
asymptomatic; can present with:
• Oliguria, nocturia, polyuria, hematuria, change
in urinary frequency
• Bone disease
• Edema, HTN, dyspnea 29
• Fatigue, depression, weakness
• Pruritus, ecchymosis
• Metallic taste in mouth, anorexia, nausea,
vomiting
• Hyperlipidemia, claudication, restless legs
• Erectile dysfunction, decrease libido, amenorrhea
30
Assessment : Physical Ecamination
• Volume status (pallor, BP/orthostatic; edema;
jugular venous distention; weight)
• Skin: sallow complexion, uremic frost
• Ammonia-like odor (uremic fetor)
31
• Cardiovascular: Assess for murmurs, bruits,
pericarditis
• Chest: pleural effusion
• Rectal: enlarged prostate
• CNS: asterixis, confusion, seizures, coma,
peripheral neuropathy
32
Evaluation
• Underlying causes may be ascertained through
clinical presentation, symptomatology, and past
medical and family history.
• ANA, antiphospholipid antibodies, C3, C4,
erythrocyte sedimentation rate (ESR) and/or C-
reactive protein (CRP) (looking for lupus
nephritis)
33
• Hepatitis panel and HIV test (looking for
infectious etiologies)
• Serum and urine protein electrophoresis
(looking for multiple myeloma) for those
patients older than age 35
• Hemoglobin A1c, fasting blood sugar, and
analysis of urine sediment.
34
BIOPSY ?
35
• Renal biopsy, if not contraindicated by
comorbidities, is indicated in patients with
unknown etiology after history and laboratory
evaluation if parenchymal disease is suspected,
or if treatment or prognosis will be based on the
biopsy.
• However biopsy is contraindicated if bilateral
small kidneys are seen on imaging, as there is a
low likelihood of improving outcome due to the
presence of late-stage disease.
36
BONES ?
37
• Increased parathyroid hormone
• Decreased 25-(OH) vitamin D
• Hypocalcemia
• Hyperphosphatemia
38
Management
39
 Correct reversible causes 
• Hypovolemia, hypotension, dehydration
• Medications (diuretics, NSAIDs, ACEI/ARB)
• Infection
• Urinary obstruction
40Case Files Family medicine, 5th edition
Lifestyle Modification
• Smoking cessation
• Weight loss
• Moderate exercise 30–60 min 4–7 d/wk
• Nutrition referral
41
AFP 2012;86:749; Ann Int Med 2013;158:825;
Kidney Int Sup 2013;3:5;
NEJM 2010;362:56
Renal Nutrition Suggestions
Factor Goal/Rational
Sodium <2 g/d. For BP and volume control
Potassium <2 g/d if hyperK, to tolerate ACEI/ARB
Glucose Low carb/sugar, if diabetic
Phosphorus
Low PO4, (↑ PO4 assoc w/ increased mortality,
vasc. Calcification)
Proteins
0.6–0.8 g/kg/d. (↑ protein diet assoc w/ ↑
mortality)
Herbal
supplements
Avoid and/or review with nephrologist before
taking
42Cochrane 2009;8:CD001892
Slowing CKD progression
• Blood Pressure Control:
Goal <130/80, <120/80 if tolerated
• Start wth ACEI (or ARB)  add diuretic 
then CCB
43
(NEJM 2015;373:2103)
ACEI or ARB
• 1st-line/renoprotective in all CKD
• tolerate 25% ↑ in Cr and K <5.5; no benefit of
ACEI + ARB combined and associated with
adverse outcomes
• 2nd-line agents include loop diuretics (if edema
present) or diltiazem/verapamil
(↓ proteinuria; antiproteinuric effect not seen
with amlodipine)
44NEJM 2004;351:1952
NEJM 2013;369:1892
Vaccines
• PSV23
• PCV13
• Influenza
• HBV 45
Cardiovascular risk reduction
• BP control
• lipids at goal
46
(Ann Int Med 2012;157:251)
Renal replacement therapy
• Includes HD, PD, transplant
• Clinical decision; consider when eGFR 5–10 &
sx of uremia/fluid overload.
• No mortality benefit to early initiation of
dialysis & no difference in CV events,
infection, HD complications
47
(CJASN 2011;6:1222)
(IDEAL, NEJM 2010;363:609)
Complications of CKD
• Anemia
• Bone Disease
• Volume Overload
• Metabolic Acidosis
48
Anemia
• Hemoglobin should be measured at least
annually in patients with stage 3 CKD, and
more frequently as renal function declines.
• There is no role for measurement of serum
erythropoietin level in the primary care
setting.
• Goal Hgb 10–11 g/dL
• correct iron deficiency before starting
epoetin/ darbepoetin
49
(NEJM 2009;361:2019)
Kidney Disease: Improving Global Outcomes (KDIGO) Anemia Work Group. KDIGO clinical
practice guideline for anemia in chronic kidney disease. Kidney Int Suppl. 2012; 2(4): 279-335.
Bone Disease
• ↓ GFR → ↑ PO4, ↓ Ca, ↓
• PO4 binder (calcium acetate, sevelamer,
lanthanum) if ↑ PO4
• 1,25-(OH) vit D (calcitriol, paricalcitol) if ↑
PTH
50(AJKD 2009;53:408)
(NEJM 2010;362:56;1312)
• Volume overload/edema: <2 g/d Na
restriction + diuretics
• Metabolic acidosis : treat w/ sodium
bicarbonate or citrate to HCO3 goal of 23–29
mEq/L; 1 tsp baking soda ≈ 6 tabs of Na-HCO3
≈ 50 mEq HCO3
51
(JAm Soc Nephrol 2015;26:515; Kidney Int 2010;78:303)
Nephrology referral
• Early referral associated with ↓ mortality.
• Refer if:
52(Am J Med 2007;120:1063)
• eGFR <30, stage 4/5 CKD;
• DM w/ mod albuminuria
(30–299 mg/d)
• Any UACR ≥300 mg/g
• ? Etiology
• rapidly ↓ GFR
• Complications of CKD
requiring Rx (i.e., Epo, PO4
binders, vit D)
• Hyperkalemia
• Resistant HTN
• Recurrent nephrolithiasis
• Suspicion of hereditary CKD
TAKE HOME MESSAGE
• Lifestyle Modification is always essential
• Never Hesitate to refer
• Tell the patient that his disease is irreversible
but can be slowed down
• Never miss the complications
53

Renal failure

  • 1.
    Renal Failure in thePrimary Care setting 1 Hasan Ismail PGY III – Family Medicine Lebanese University
  • 2.
    Objectives • To identifythe role of the Family Physician in the management of CKD • To be aware of referral indications • To be able to treat and follow most of the CKD complications 2
  • 3.
    • A 46-year-oldwoman - First visit • CC :Decreased urinary output for 5 months with a foamy appearance. • Swelling in both legs • non bloody, non bilious emesis a few times a week. 3 Case scenario 1
  • 4.
    • Diet: “Ieat the best I can for what I afford but often have very little appetite” 4 • Diabetes since 10 years ago and has been taking insulin for 2 years. • She does not check her sugars at home because she does not like to "stick" herself.
  • 5.
    • Obese • Hertemperature is 37.2°C, her heart rate is • 108 beats/min, her blood pressure is 198/105 mm Hg, her respiration is 19 breaths/ • min, and her oxygen saturation is 94% on room air. • (HEENT) examination reveals periorbital edema. • Her skin is hyperpigmented on both lower extremities. 5
  • 6.
    • Tachycardia withan S1, S2, S4 gallop, Vesicular breath • No jugular venous distension and no carotid bruits. • Abdomen is nontender, with no bruits or masses palpated. • The lower extremities reveal pitting pretibial edema with a pit recovery time less than 40 seconds. 6
  • 7.
    Labs • Urinalysis  Hyalinecasts  3+ proteinuria  Glucose  negative for ketones. • Her hemoglobin is 10.9 g/dl and her hematocrit is 32% with a mean corpuscular volume (MCV) of 82.3 g/dl. 7
  • 8.
    Case 1 Summary •This is a 46-year-old woman with chronic kidney disease (CKD). She has a history of uncontrolled diabetes and currently has uncontrolled hypertension. • She presents with periorbital edema, long- standing lower-extremity edema, an S4 and central obesity. • The urinalysis shows hyaline casts, • 3+ proteinuria and glucose, negative ketones, and hemoglobin 10.9 g/dL with an MCV of82.3 g/dL. 8
  • 9.
    What is yournext diagnostic step? 9
  • 10.
    • serum electrolytes •blood urea nitrogen (BUN) • Creatinine • imaging of the kidneys 10
  • 11.
    Next step intherapy ? 11
  • 12.
    • Further historyto identify and remove any offending agents (such as nonsteroidal anti- inflammatory drugs [NSAIDs]) • Control of blood pressure and diabetes • May require dialysis if she develops complications such as pulmonary edema, severe hyperkalemia, or anuria 12
  • 13.
    • A significantreduction in urine output requires immediate evaluation of creatinine function and volume status. • Volume status is assessed by skin turgor, mucous membranes, specific gravity in the urinalysis, and orthostatic blood pressure. • A low volume status with an elevated creatinine requires that the patient be given IV fluids to see if there can be any recovery of kidney function. 13
  • 14.
    • The patient'suncontrolled diabetes and hypertension predispose her to kidney damage. • Another common offender is a patient with this history who is taking NSAIDs. • This will increase the patient's already high risk of damage. 14
  • 15.
    Etiologies • DM, HTN,and glomerulonephritis. • Diabetic kidney disease occurs in 30% to 40% of type I DM, in 25% of type II DM, and in 24% of HTN patients. • 20% to 60% of DM patient are HTN ! •  Many patients present at a later stage of CKD and it is then difficult to determine the etiology 15
  • 16.
    16 Davidson’s Principles andpractice of medicine, 23rd edition
  • 17.
    • Progressive destructionof nephrons; • GFR will drop gradually, and plasma Cr values will approximately double, with 50% reduction in GFR and 75% loss of functioning nephrons mass. • Hyperkalemia usually develops when GFR falls to <20 to 25 mL/min 17
  • 18.
  • 19.
    • USPSTF 2012 -Insufficient evidence to recommend for or against routine screening. • ACP 2013, AAFP 2014 - Do not screen adults unless they have symptoms or risk factors. - Adults taking an ACE inhibitor or ARB should not be tested for proteinuria, regardless of diabetes status. 19 * USPSTF. Chronic Kidney Disease (CKD): Screening. 2012. ** AAFP Clinical Recommendations: Chronic Kidney Disease. 2014. Ann Intern Med. 2013;159(12):835
  • 20.
    • NICE 2014 -Monitor glomerular filtration rate (GFR) at least annually in people prescribed drugs known to be nephrotoxic (calcineurin inhibitors, lithium, or nonsteroidal anti-inflammatory drugs (NSAIDs)..) - Screen renal function in people at risk for CKD (DM, HTN, CVD, structural renal disease, nephrolithiasis, BPH, multisystem diseases with potential kidney involvement, stage 5 CKD or hereditary kidney disease, or personal history of hematuria or proteinuria 20Early identification and management of chronic kidney disease in adults in primary and secondary care. London (UK): NICE; 2014
  • 21.
  • 22.
    22 serum creatinine Estimation ofGFR Urine albumin/ creatinine ratio Urinalysis
  • 23.
    Definition ≥3 mo w/GFR <60 mL/min/1.73 m2 or signs of kidney damage: Proteinuria/albuminuria, pathology on renal biopsy/imaging 23 Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013; 3(1): 1-150.
  • 24.
  • 25.
    Albuminuria Stage 25 based onalbuminuria (mg/d) or spot urine Alb/Cr (mg) ratio (ACR): • A1: nl or mildly ↑ (ACR <30) • A2: mod ↑ [formerly microalbuminuria] (ACR 30–299) • A3: or severely ↑ [formerly macroalbinuria] (ACR ≥300) (Kid Int 2013;3:19)
  • 26.
    Geriatric Considerations • GFRnormally decreases with age, despite normal creatinine (Cr). • Adjust renally cleared drugs for GFR in the elderly. 26
  • 27.
    Pediatric Considerations • CKDdefinition is not applicable for children <2 years because of lower GFR even when corrected for body surface area. • Calculated GFR based on serum Cr is used in this age group. 27
  • 28.
    Pregnancy Considerations • Renalfunction in CKD may deteriorate during pregnancy. • Cr >1.5 and hypertension (HTN) are major risk factors for worsening renal function. • Increased risk of premature labor, preeclampsia, and/or fetal loss • ACE inhibitors and angiotensin receptor blockers (ARBs) are contraindicated due to teratogenicity. • Use diuretics with caution 28
  • 29.
    Assessment : Historytaking Patients with CKD stages 1 to 3 are usually asymptomatic; can present with: • Oliguria, nocturia, polyuria, hematuria, change in urinary frequency • Bone disease • Edema, HTN, dyspnea 29
  • 30.
    • Fatigue, depression,weakness • Pruritus, ecchymosis • Metallic taste in mouth, anorexia, nausea, vomiting • Hyperlipidemia, claudication, restless legs • Erectile dysfunction, decrease libido, amenorrhea 30
  • 31.
    Assessment : PhysicalEcamination • Volume status (pallor, BP/orthostatic; edema; jugular venous distention; weight) • Skin: sallow complexion, uremic frost • Ammonia-like odor (uremic fetor) 31
  • 32.
    • Cardiovascular: Assessfor murmurs, bruits, pericarditis • Chest: pleural effusion • Rectal: enlarged prostate • CNS: asterixis, confusion, seizures, coma, peripheral neuropathy 32
  • 33.
    Evaluation • Underlying causesmay be ascertained through clinical presentation, symptomatology, and past medical and family history. • ANA, antiphospholipid antibodies, C3, C4, erythrocyte sedimentation rate (ESR) and/or C- reactive protein (CRP) (looking for lupus nephritis) 33
  • 34.
    • Hepatitis paneland HIV test (looking for infectious etiologies) • Serum and urine protein electrophoresis (looking for multiple myeloma) for those patients older than age 35 • Hemoglobin A1c, fasting blood sugar, and analysis of urine sediment. 34
  • 35.
  • 36.
    • Renal biopsy,if not contraindicated by comorbidities, is indicated in patients with unknown etiology after history and laboratory evaluation if parenchymal disease is suspected, or if treatment or prognosis will be based on the biopsy. • However biopsy is contraindicated if bilateral small kidneys are seen on imaging, as there is a low likelihood of improving outcome due to the presence of late-stage disease. 36
  • 37.
  • 38.
    • Increased parathyroidhormone • Decreased 25-(OH) vitamin D • Hypocalcemia • Hyperphosphatemia 38
  • 39.
  • 40.
     Correct reversiblecauses  • Hypovolemia, hypotension, dehydration • Medications (diuretics, NSAIDs, ACEI/ARB) • Infection • Urinary obstruction 40Case Files Family medicine, 5th edition
  • 41.
    Lifestyle Modification • Smokingcessation • Weight loss • Moderate exercise 30–60 min 4–7 d/wk • Nutrition referral 41 AFP 2012;86:749; Ann Int Med 2013;158:825; Kidney Int Sup 2013;3:5; NEJM 2010;362:56
  • 42.
    Renal Nutrition Suggestions FactorGoal/Rational Sodium <2 g/d. For BP and volume control Potassium <2 g/d if hyperK, to tolerate ACEI/ARB Glucose Low carb/sugar, if diabetic Phosphorus Low PO4, (↑ PO4 assoc w/ increased mortality, vasc. Calcification) Proteins 0.6–0.8 g/kg/d. (↑ protein diet assoc w/ ↑ mortality) Herbal supplements Avoid and/or review with nephrologist before taking 42Cochrane 2009;8:CD001892
  • 43.
    Slowing CKD progression •Blood Pressure Control: Goal <130/80, <120/80 if tolerated • Start wth ACEI (or ARB)  add diuretic  then CCB 43 (NEJM 2015;373:2103)
  • 44.
    ACEI or ARB •1st-line/renoprotective in all CKD • tolerate 25% ↑ in Cr and K <5.5; no benefit of ACEI + ARB combined and associated with adverse outcomes • 2nd-line agents include loop diuretics (if edema present) or diltiazem/verapamil (↓ proteinuria; antiproteinuric effect not seen with amlodipine) 44NEJM 2004;351:1952 NEJM 2013;369:1892
  • 45.
  • 46.
    Cardiovascular risk reduction •BP control • lipids at goal 46 (Ann Int Med 2012;157:251)
  • 47.
    Renal replacement therapy •Includes HD, PD, transplant • Clinical decision; consider when eGFR 5–10 & sx of uremia/fluid overload. • No mortality benefit to early initiation of dialysis & no difference in CV events, infection, HD complications 47 (CJASN 2011;6:1222) (IDEAL, NEJM 2010;363:609)
  • 48.
    Complications of CKD •Anemia • Bone Disease • Volume Overload • Metabolic Acidosis 48
  • 49.
    Anemia • Hemoglobin shouldbe measured at least annually in patients with stage 3 CKD, and more frequently as renal function declines. • There is no role for measurement of serum erythropoietin level in the primary care setting. • Goal Hgb 10–11 g/dL • correct iron deficiency before starting epoetin/ darbepoetin 49 (NEJM 2009;361:2019) Kidney Disease: Improving Global Outcomes (KDIGO) Anemia Work Group. KDIGO clinical practice guideline for anemia in chronic kidney disease. Kidney Int Suppl. 2012; 2(4): 279-335.
  • 50.
    Bone Disease • ↓GFR → ↑ PO4, ↓ Ca, ↓ • PO4 binder (calcium acetate, sevelamer, lanthanum) if ↑ PO4 • 1,25-(OH) vit D (calcitriol, paricalcitol) if ↑ PTH 50(AJKD 2009;53:408) (NEJM 2010;362:56;1312)
  • 51.
    • Volume overload/edema:<2 g/d Na restriction + diuretics • Metabolic acidosis : treat w/ sodium bicarbonate or citrate to HCO3 goal of 23–29 mEq/L; 1 tsp baking soda ≈ 6 tabs of Na-HCO3 ≈ 50 mEq HCO3 51 (JAm Soc Nephrol 2015;26:515; Kidney Int 2010;78:303)
  • 52.
    Nephrology referral • Earlyreferral associated with ↓ mortality. • Refer if: 52(Am J Med 2007;120:1063) • eGFR <30, stage 4/5 CKD; • DM w/ mod albuminuria (30–299 mg/d) • Any UACR ≥300 mg/g • ? Etiology • rapidly ↓ GFR • Complications of CKD requiring Rx (i.e., Epo, PO4 binders, vit D) • Hyperkalemia • Resistant HTN • Recurrent nephrolithiasis • Suspicion of hereditary CKD
  • 53.
    TAKE HOME MESSAGE •Lifestyle Modification is always essential • Never Hesitate to refer • Tell the patient that his disease is irreversible but can be slowed down • Never miss the complications 53