How to retard the progression of ckd

1. How to retard the progression ofHow to retard the progression of
CKD?CKD?
Tarek Mohamed El TantawyTarek Mohamed El Tantawy
MD, MSc Nephrology – Ain Shams UniversityMD, MSc Nephrology – Ain Shams University
Egyptian Nephrology Fellowship Trainer – MNGHEgyptian Nephrology Fellowship Trainer – MNGH
Secretary-General of the Dakhlia Nephrology GroupSecretary-General of the Dakhlia Nephrology Group
HQM – CambridgeHQM – Cambridge

2.  Introduction.
 CKD definition and classification.
 CKD Biomarkers.
 Risk factors for CKD progression.
 Interventions to slow CKD progression.
 Conclusion.
Agenda

3.  The management of progression of CKD is aimed at addressing a multiplicity
of factors known to be associated with progression.
 There are general measures which have been shown to address cardiovascular
health and CKD. Addressing CVD risk factors may indirectly and directly
impact CKD progression.
 Strategies include general lifestyle measures which improve cardiovascular
health, BP control, and interruption of the RAAS.
 In addition, control of other metabolic parameters such as blood sugar, uricblood sugar, uric
acid, acidosis, and dyslipidemia together with cessation of smokingacid, acidosis, and dyslipidemia together with cessation of smoking may also
be important.
Introduction

4. -CKD is defined as either:
-kidney damage (proteinuria, hematuria, or structural abnormalities of the
kidney) with or without impaired GFR
or impaired GFR < 60 ml/min per 1.73m² with or without kidney damage
that persists for > 3 monthsthat persists for > 3 months. KDIGO guidelines
4

5.  Albuminuria and eGFR provide independent information regarding risk of
CKD progression, AKI , cardiovascular disease, and mortality.
CKD Classification

6.  KDIGO recommends classification based on Cause, GFR category, and Albumin
category (referred to as CGA). Cause is added because it provides important
prognostic information, as well as influences treatment decisions.
 The KDIGO guideline recommends that the cause of CKD be based on the
presence or absence of systemic disease (e.g., diabetes, lupus) and the anatomic
location of the pathologic abnormalities within the kidney (e.g., glomerular,
tubulointerstitial diseases, vascular diseases, cystic and congenital diseases).
CKD classification
CGA

7.  Ideal urinary and plasmaurinary and plasma biomarkers for CKD would identify patients who develop
progressive CKD, monitor effects of treatment, and be useful and convenient in clinical
practice.
 UrinaryUrinary albuminalbumin is a good example, although some patients will progress despite
normoalbuminurianormoalbuminuria.
 Other CKD biomarkers include markers of tubular damagemarkers of tubular damage ,those that reflect early
inflammation/fibrosis, markers of mineral bone diseasemarkers of mineral bone disease, and natriuretic hormonesnatriuretic hormones.
 O’Seaghdha et al., 2011 found that lower urinary connective tissue growth factorlower urinary connective tissue growth factor
levels were associated with incident CKD.
 Dieplinger et al., 2009 found that A-type natriuretic peptideA-type natriuretic peptide and adrenomedullinadrenomedullin
plasma concentrations predict progression of nondiabetic kidney disease.
 Large prospective studies are required to validate biomarkers, and establish threshold
values for prediction of CKD progression; none of these biomarkers are presently readynone of these biomarkers are presently ready
for clinical use.for clinical use.
CKD Biomarkers

8.  proteinuria is an independent risk for renal outcomes regardless of eGFR.
 The Chronic Kidney Disease Prognosis Consortium examined a collaborative
meta-analysis, from 45 studies > 1,555,332 patients were examined and included
those in the general population, at high risk, and with CKD.
 A higher relative risk for progressive CKD and ESRD was associated with both
lower eGFR levels and higher levels of albuminuria.
 Increased risk for mortality and adverse renal outcomes was statistically
significant for urine ACR > 30 mg/g, even when eGFR was > 60 ml/min per
1.73m² , consistent with the current threshold value for albuminuria (> 30 mg/g) as
a marker of kidney damage.
 The relative risk for ESRD in a patient with an eGFR of 60 to 75 ml/min per
1.73m² and an ACR ≥ 300 mg/g is greater than a patient with an eGFR of 30 to 45
ml/min per 1.73m² with an ACR < 10 mg/g (relative risk of 67 versus 56).
Risk factors for CKD progression
Proteinuria

9.  Obesity may contribute to both incident CKD and increased CKD progression
by increasedincreased insulin resistance and sympathetic activity, activation of theinsulin resistance and sympathetic activity, activation of the
RAAS with local renin angiotensin and aldosterone synthesis in adipose tissue,RAAS with local renin angiotensin and aldosterone synthesis in adipose tissue,
and increased inflammatory adipose-based cytokines such as leptin andand increased inflammatory adipose-based cytokines such as leptin and
adiponectinadiponectin.
 Significant proteinuria and obesity was associated with CKD progression and
ACE inhibition was more renoprotective in obese patients, possibly due to
inhibition of the enhanced baseline renin, angiotensin, and aldosterone levels
in these individuals.
 Obesity is associated with secondary focal and segmental glomerulosclerosis.secondary focal and segmental glomerulosclerosis.
Risk factors for CKD progression
Obesity

10.  11 studies of >30,000 participants
showed that metabolic syndrome
was associated with a 55%
increased risk for the development
of eGFR <60 ml/min per 1.73 m².
 For individual components of the
metabolic syndrome, the OR of
developing an eGFR < 60 ml/min
per 1.73 m² were 1.61 for elevated
BP, 1.27 for elevated triglycerides,
1.23 for low HDL cholesterol, 1.19
for abdominal obesity, and 1.14 for
impaired fasting glucose.
Risk factors for CKD progression
Metabolic Syndrome

11.  In patients with normal albumin excretion, the traditional BP goal of < 130/80< 130/80
mmHg in CKD patients did not slow the progression compared with < 140/90< 140/90
mmHg . Those with albumin excretion > 300> 300 mg/d may benefit from the lower
target < 130/ 80< 130/ 80 mmHg.
 In patients with proteinuric CKD ( >300 mg/d ),( >300 mg/d ), inhibition of the RAAS is
superior to other antihypertensive medications in slowing CKD progression.
However, in those with less proteinuria, it is not clear which class of
antihypertensive agents is most beneficial.
 ACEIs combined with ARBs showed no benefit in preventing progression of
microalbuminuria or ESRD over either medication alone in a systematicsystematic
review of randomized controlled trials.review of randomized controlled trials.
Risk factors for CKD progression
Hypertension

12.  The relationship between systolic, diastolic, and pulse pressure with ESRD
risk was assessed in > 16,000 Kidney Early Evaluation Program study
participants (2012) with an eGFR of < 60 ml/min per 1.73m².
 After adjustment for demographics, comorbidities, BMI, eGFR, and
albuminuria.
 High Systolic BP accounted for most of the risk of progression to ESRD.
There was a significant 36%36% increased risk for ESRD in participants with a
Systolic BPSystolic BP ≥≥ 150 mmHg.150 mmHg.
 Persons with Diastolic BP > 90Diastolic BP > 90 mmHg were at 81%81% higher risk for ESRD
compared with those with Diastolic BP of < 80 mmHg.
 Higher pulse pressure (> 80 mmHg versus < 50 mmHg) was not associated
with ESRD after adjustment for SBP.
Risk factors for CKD progression
Hypertension
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13.  CKD progression may increase with cardiac dysfunction by decreased renaldecreased renal
perfusion, increased renal venous pressure, increased endothelial dysfunction,perfusion, increased renal venous pressure, increased endothelial dysfunction,
and altered neurohormonal factors.and altered neurohormonal factors.
Risk factors for CKD progression
Cardiovascular Abnormalities

14.  The cardiac concentricity” the ratio of left ventricular mass to left ventricularthe ratio of left ventricular mass to left ventricular
end-diastolic volume,end-diastolic volume, an early sensitive measure ofearly sensitive measure of cardiac remodelingcardiac remodeling”
was associated with renal function decline.
 Atrial fibrillationAtrial fibrillation is common in CKD and has been reported in up to 20%
of CKD patients.
 Takahashi et al., 2011 compared eGFR values before and 1 year after catheter
ablation for atrial fibrillation in 386 Japanese patients.
• Baseline eGFR was 68 ml/min per 1.73 m² and 26% of patients had stage 3
CKD.
• The 72% of patients who remained free from arrhythmias over the 1-year
follow-up had a significant 3 ml/min per 1.73 m² increase in eGFR, whereas
those with recurrent arrhythmias had a 2 ml/min per 1.73 m² decrease
compared with baseline.
Risk factors for CKD progression
Cardiovascular Abnormalities

15.  The role of uric acid as either a causal factor or as a marker of CKD is controversial.
 Proposed mechanisms for uric acid induced kidney damage include hypertension,hypertension,
with activation of the RAAS, renal afferent arteriolopathy, increased glomerularwith activation of the RAAS, renal afferent arteriolopathy, increased glomerular
hydrostatic pressure, and fibrosis.hydrostatic pressure, and fibrosis.
 Bellomo et al.,2010 examined 900 healthy blood donors who had a serum uric acid
measurement, and followed up with a serum creatinine 5 years later; those with an
ACR > 300 mg/g Cr were excluded. The adjusted HR for loss of eGFR >10 ml/min
per 1.73m² was 1.28 for every 1 mg/dl increase in serum uric acid. The eGFR
decline was seen in men with serum uric acid ≥ 5.5 and for women ≥ 5 mg/dl.
 Madero et al., 2010 who examined the association of baseline serum uric acid level
with death and renal failure in 840 participants of the MDRD study over a median
follow-up of 10 years. The mean measured GFR was33 ml/min per 1.73m² with
median serum uric acid of 7.6 mg/dl in participants of the study. The highest tertile
of serum uric acid ( 8.4 to 15.6 ) was associated with death (HR 1.57), but not with
kidney failure.
Risk Factors for CKD Progression
Hyperuricemia

16.  There is insufficient evidence to support or refute the use of agents to lower
serum uric acid concentrations in people with CKD and either symptomatic or
asymptomatic hyperuricemia in order to delay progression of CKD. (Not
Graded)
 Treatment of asymptomatic hyperuricemia has also been reported to improve
kidney function even in subjects with normal levels of GFR. Both GFR and
endothelial function significantly improved in asymptomatic hyperuricemic
subjects randomly assigned to 300 mg/day of allopurinol in comparison to
placebo.
 Other uric acid lowering agents have also been reported to improve outcomes
in people with CKD. In an 8-week, placebo-controlled group comparison of
rasburicase and placebo, a single 4.5 mg dose of rasburicase significantly
lowered serum uric acid and resulted in a significant improvement in kidney
function assessed by CrCl.
Risk Factors For CKD Progression
Hyperuricemia – KDIGO 2013

17.  Elevated serum phosphate appears to play a role in CKD progression rather
than simply being consequences of CKD.
 Zoccali et al., 2011 examined the relationship between serum phosphate and
CKD progression in 331 participants in the REIN trial.
• In both the ramipril and placebo groups, those who had serum phosphate levels
in the upper two quartiles progressed faster to ESRD or to the combined
endpoint of ESRD and doubling of serum creatinine.
• Higher serum phosphate levels decreased the renoprotective effects of
ramipril.
• One limitation of this study is that it did not have FGF-23 measurements.
Risk factors for CKD progression
Phosphates

18.  FGF-23 levels rise in CKD to increase urinary phosphate excretion to maintain normal
serum phosphate levels.
 FGF-23 is a biomarker for CKD, its levels increase before increases in serum phosphate
or parathyroid hormone levels.
 FGF-23 may cause kidney injury indirectly by reducing 1,25(OH)2 vitamin D levels, or
directly via an unknown mechanism similar to the cardiac toxicity (LVH).
 Isakova et al., 2011 examined the association of FGF-23 levels with both mortality
and ESRD in patients with CKD in the Chronic Renal Insufficiency Cohort study.
• This study included nearly 3800 patients with stage 2–4 CKD, with 89% having normal
phosphate levels. The mean FGF-23 level was 145.5 RU/ml (versus a reference median
of 43 RU/ml in a non-CKD population).
• During 3.5 years of follow-up, 266 patients died and 410 reached ESRD.
• Elevated FGF-23 was independently associated with death, but there was a more
complex relationship with progression to ESRD.
Risk factors for CKD progression
FGF-23

19.  AKI is a risk factor for CKD progression and severity of AKI predicts worse
outcomes. Those who required dialysis for AKI had a 500-fold increased
likelihood for developing stage 4 CKD
 Even complete recovery from AKI within 10% of baseline values leads to
increased CKD incidence/progression and should be followed by a nephrologist.
 Coca et al., 2012 conducted a systematic review of the incidence and relative risks of
these long term consequences of patients with and without AKI.
 Pooled data from 13 studies of >1.4 million people showed that the incidence of CKD and
ESRD were 25.8 per 100 person-years and 8.6 per 100 person-years, respectively, in
individuals with AKI.
 The pooled hazard ratios for patients who had AKI for subsequent CKD, ESRD, and death
were 8.8 (95% CI, 3.1–25.5), 3.1 (95% CI, 1.9–5.0), and 2.0 (95% CI, 1.3–3.1),
respectively, compared with patients without AKI.
Risk factors for CKD progression
Acute Kidney Injury

20.  Identifying genetic variants associated with CKD would be important for
identifying those at risk, predicting progression, possibly initiating early therapy,
and understanding the pathophysiology of CKD.
 There is an increased risk for ESRD in African AmericansAfrican Americans.
 Genovese et al., 2010 described the finding of two risk alleles in the coding
region of apolipoprotein A1apolipoprotein A1 (found on chromosome 22chromosome 22) that are associated with
FSGS and hypertensive ESRD in African AmericansFSGS and hypertensive ESRD in African Americans.
• The association of “ApoL1ApoL1” with hypertensive ESRD was tested in
approximately 1,000 African American cases and 1,000 controls and these alleles
were strongly associated with hypertensivehypertensive ESRDESRD.
• The odds ratio for 2 “ApoL1” risk alleles was 7.3 versus 0 alleles and 5.8 versus
1 allele for hypertensive ESRD.
Risk factors for CKD progression
Genetics

21.  Race and genetics represent two important nonmodifiable risk factors for
progression.
 Blacks and Hispanics with more African ancestry have an increased risk of CKD,
which starts before an eGFR <60 ml/min per 1.73 m².
 ApoL1ApoL1 risk alleles, low birth weightlow birth weight, and socioeconomicsocioeconomic factorsfactors and poorerpoorer
accessaccess to health careto health care may all play roles in faster progression in blacks.
Risk factors for CKD progression
Race and Socioeconomic Status

22.  Nephrolithiasis may increase CKD progression by interstitial calcificationsinterstitial calcifications,
crystallization in tubulescrystallization in tubules, repeated urinary obstructionrepeated urinary obstruction, and lithotripsylithotripsy, which
may cause parenchymal damage.
 Alexander et al., 2012 examined the association of new kidney stones with CKD
progression in a large registry cohort. Patients with pyelonephritis were
excluded.
• >23,700 patients with at least one kidney stone, 5333 patients developed ESRD.
• Having one or more stones was associated with two-fold increasedtwo-fold increased risk of ESRD,
new stage 3b–5 CKD, and doubling of serum creatinine compared with those
without kidney stones during 11 years of follow-up.
• The excess risk of stones seemed greater in women and in individuals aged <50
years.
Risk Factors for CKD progression
Nephrolithiasis

23.  Solitary cysts are not normally thought to affect kidney function.
• It was postulated that tubular epithelial injury may lead to cyst formation, and
that cysts could be markers of prior tubular damage.
• Cysts were associated with albuminuria in a single study “Rule et al; 2012 ”.
 Isolated microscopic hematuria without proteinuria revealed ” renal biopsies”
that many of these patients had IgA nephropathy, thin basement membraneIgA nephropathy, thin basement membrane
disease, MPGN, or Alport syndromedisease, MPGN, or Alport syndrome, none of which have specific therapy.
• Vivante et al; 2011 designed a large cohort study revealed that isolated
microscopic hematuria with < 200mg/d of proteinuria is associated with
increased ESRD risk.
Risk Factors for CKD progression
Renal cysts – Isolated microscopic hematuria

24.  Cigarette smoking is associated with abnormalabnormal urine albuminurine albumin and progression
of CKD.
 Smoking is an important renal risk factor, and nephrologists have to invest
more efforts to motivate patients to stop smoking. Smoking cessationSmoking cessation
improves oxygen delivery to the glomeruli.improves oxygen delivery to the glomeruli.
 Multiple studies document a clear association between smoking and renal
damage in the general population, patients with diabetes, and hypertensive
patients.
 Studies investigating the beneficial effects of smoking cessation on kidney
function have all been positive.
Miscellaneous RF for CKD progression
Smoking- KDIGO 2013

25. Interventions to Slow CKD Progression

26.  We recommend that people with CKD be encouraged to undertake physical activity
compatible with cardiovascular health and tolerance (aiming for at least 30 minutes 5
times per week), achieve a healthy weight (BMI 20 to 25), and stop smoking. (1D)
 Frailty, impaired physical performanceFrailty, impaired physical performance, disabilitydisability, and geriatric syndromesgeriatric syndromes are common
among older adults even with mild kidney disease.
 CKD patients have a reduced exercise capacity and impaired physical functioning.
Moreover, reduced physical activity is associated with increased mortality and poorincreased mortality and poor
QOL in people with CKD.QOL in people with CKD.
 Regular exercise leads to increased exercise capacity, decreased morbidity, andto increased exercise capacity, decreased morbidity, and
improved health-related QOLimproved health-related QOL. Exercise may reduce cardiovascular riskreduce cardiovascular risk through its
beneficial effects on BP, triglycerides, high-density lipoprotein cholesterol , insulinBP, triglycerides, high-density lipoprotein cholesterol , insulin
resistance, and glycemic controlresistance, and glycemic control.
 In ESRD, exercise has been shown to improveimprove arterialarterial stiffnessstiffness, BPBP, cardiorespiratorycardiorespiratory
function, and QOL.function, and QOL.
Interventions to Slow CKD Progression
Lifestyle - KDIGO 2013

27.  Dietary sodium restriction has traditionally been advocated for the beneficial
effects on hypertension and assumed benefits of improved outcomes regarding
CKD progression.
 However, there has been recent controversy regarding the expected benefits
versus possible harms from dietary sodium restriction. Dietary sodiumDietary sodium
restriction could result in an increased activity of the renin-angiotensin-restriction could result in an increased activity of the renin-angiotensin-
aldosterone system, increased sympathetic activity, and insulin resistance, allaldosterone system, increased sympathetic activity, and insulin resistance, all
of which might worsen CKD progression.of which might worsen CKD progression.
 The optimal dietary sodium intake for slowing CKD progression remains
unclear. For those patients with moderate CKD and heavy proteinuria, high
dietary sodium intake may worsen CKD progression.
 The present recommendation of 2500 mg of sodium intake per day for
hypertensive patients is reasonable, but extremely low dietary sodium intakes
(<1250mg/d) should possibly be avoided.
Interventions to Slow CKD Progression
Low Sodium Diet

28.  We recommend a target HbA1c of ~7.0% to prevent or delay progression of theprevent or delay progression of the
microvascular complications of diabetes, including diabetic kidney disease.microvascular complications of diabetes, including diabetic kidney disease. (1A)
 We recommend not treating to an HbA1c target of < 7.0% in patients at risk of
hypoglycemia, this risk will be higher in people with lower levels of kidney function.
(1B)
 We suggest that target HbA1c be extended above 7.0% in individuals with
comorbidities or limited life expectancy and risk of hypoglycemia. (2C)
 In people with CKD and diabetes, glycemic control should be part of a multifactorial
intervention strategy addressing blood pressure control and cardiovascular risk,
promoting the use of ACEI or ARB, statins, and antiplatelet therapy where clinically
indicated. (Not Graded)
Interventions to Slow CKD Progression
Glycemic control (NKF) KDOQI 2012

29.  Fluid intake may influence CKD incidence because a high intake may help
increase solute clearance and prevent kidney stonesincrease solute clearance and prevent kidney stones. Conversely, lower fluid
intake with resulting urinary concentration may increase the metabolic
demand of the kidneys.
 Clark et al., 2011 assessed the effect of increased fluid intake on incident
CKD and kidney function decline in a 6-year, prospective cohort study of
>2100 participants.
• These participants had to have a baseline eGFR >60 ml/min per 1.73 m². Valid
24-hour urine samples were collected and participants were grouped in
categories of < 1 L/d, 1–1.9 L/d, 2–2.9 L/d, and >3 L/d.
• Annual eGFR decline was progressively slower, from 1.3%, to 1.0%, to 0.8%,
and to 0.5%, respectively (P = 0.02).
 it seems reasonable to recommend a higher fluid intake of 2–32–3 L/d in patients
with risk factors for CKD if there are no contraindicationsno contraindications.
Interventions to Slow CKD Progression
Fluid Intake

30.  A low protein diet has been advocated to slow the progression of CKD. Unfortunately,
the MDRD study was unable to show conclusive benefit of a low protein diet (0.58
g/kg/d) versus a very low protein diet (0.28 g/kg/d) supplemented with essential
ketoacids and amino acids in slowing non-diabetic CKD.
 Menon et al., 2009 examined the long-term effects between these two diets used in the
MDRD initial trial in 255 individuals with measured GFR values between 13 to 24
ml/min per 1.73m² who continued in a long term follow-up study with no dietary
recommendations.
• Outcomes measured were ESRD, death, and the composite of both. In the low protein
diet group, 90.7% reached kidney failure compared to 87.3% in the very low protein
diet group. The composite end point was reached in 96.1% in the low protein group
versus 95.2% in the very low protein group. However, 23.3% died in the low protein
group compared to 38.9% in the very low protein group.
• The very low protein diet did not delay progression to kidney failure compared to theThe very low protein diet did not delay progression to kidney failure compared to the
low protein diet, but appeared to increase the risk of death.low protein diet, but appeared to increase the risk of death.
Interventions to Slow CKD Progression
Low Protein Diet

31.  Nath et al., 2012 showed that, with CKD, increased single nephron ammoniasingle nephron ammonia
genesis can activate the alternative complement system and lead togenesis can activate the alternative complement system and lead to
tubulointerstitial inflammation and injury.tubulointerstitial inflammation and injury.
 Shah et al., 2012 performed a retrospective cohort study of over 5,422
outpatients with a mean age of 52 years; 69% were women, 45% were African
American, 21% had diabetes, 41% had hypertension, and 9% had an
eGFR< 60 ml/min per 1.73m². Kidney disease progressed in 6.2% as defined
by a decrease in eGFR by 50% or reaching an eGFR< 15 ml/min per 1.73m²
during follow-up.
• After adjustments for baseline eGFR, clinical, and demographic factors,
individuals with a baseline serum bicarbonate < 22 mEq/L< 22 mEq/L had a hazard ratio
of 1.541.54 for developing progressive kidney disease compared to those with
baseline serum bicarbonate levels of 25 to 2625 to 26 mEq/L.
• Alkali may have beneficial effects by decreasing tubulointerstitial damage.Alkali may have beneficial effects by decreasing tubulointerstitial damage.
Interventions to Slow CKD Progression
Oral Alkali for Metabolic Acidosis

32.  The potential beneficial effects of vitamin D on CKD
progression include inhibiting the renin angiotensininhibiting the renin angiotensin
systemsystem at multiple steps, having anti-inflammatoryanti-inflammatory
propertiesproperties, and reducing podocyte injuryreducing podocyte injury.
 Fishbane et al., 2013 studied the effects of paricalcitol1g/d on
proteinuria in 61 proteinuric CKD patients in a randomized,
placebo-controlled double blind, 6-month study.
• The paricalcitol group had a significant decrease in proteinuria ofdecrease in proteinuria of
17.6%17.6% from baseline compared to controls where there was a 2.9%
increase.
Interventions to Slow CKD Progression
Paricalcitol

33. Proper hydration 2-3 L /day if there are no contraindicationsno contraindications.
Avoiding Drugs such as Aminoglycosides, NSAIDs.
Avoiding exposure to radio - contrast agents.
In presence of dehydration, even in absence of renovascular
disease, ACEIs or ARBs can aggravate renal dysfunction.
Dehydration is frequent in tubulo - interstitial disorders where
urinary concentration is impaired.
Proper Dosing of Drugs eg. Allopurinol, digoxin
Interventions to Slow CKD Progression
Avoidance of Dehydration/Nephrotoxic Agents

34.  Although CKD is generally progressive and irreversible, there are steps
providers and patients can take to slow progression, enabling patients to
live longer without complications or the need for renal replacement
therapy.
 BP control, reduction of proteinuria, RAAS inhibition and in patients
with diabetes, glycemic control have been traditional strategies
employed to slow progression of CKD.
 Other factors that may influence or predict CKD progression, such as
biomarkers, genetics, race, acidosis, uric acid, diet, kidney stones, and
acute kidney injury.
 Trials to slow CKD progression using certain antihypertensive agents,
oral alkali, allopurinol, low salt &protein diets, paricalcitol and prompt
glycemic control with avoidance of dehydration and nephrotoxic drugs.
CONCLUSIONS

35. THANK YOUTHANK YOU