This document discusses chronic kidney disease (CKD) in 3 sentences: CKD is defined as kidney damage or decreased kidney function lasting over 3 months that leads to a progressive loss of kidney function and mass over time. CKD has many risk factors including diabetes, hypertension, family history, and is a global epidemic associated with high costs. The management of CKD focuses on monitoring kidney function, preventing progression, treating complications like anemia and bone disease, controlling cardiovascular risk factors, and preparing for renal replacement therapies like dialysis.

1. Chronic kidney disease(CKD)
-Dr. Anjani kumar jha
-Resident
-Internal medicine

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3. Contents
• Definition
• Risk factors and Etiology
• Pathophysiology
• Clinical features
• Investigations
• Management
-Expected duration-45mins
-Number of slides-
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4. Definition
• Chronic kidney disease refers to an irreversible
deterioration in renal function that usually
develops over a period of years.
• Initially it manifests only as a biochemical
abnormality but , eventually , loss of the excretory
, metabolic and endocrine functions of the kidney
leads to the clinical symptoms and signs of renal
failure collectively referred to as uraemia.
• When death is likely without RRT ( CKD stage 5)
it is called end stage renal disease(ESRD).
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5. Contd..
• According to NHRC, Assessment of CKD
support program of GoN 2016 ; CKD is
defined as renal damage or decreased renal
function for 3 or more months along with
progressive destruction of renal mass with
irreversible sclerosis and loss of nephrons.
• It is a global epidemic associated with high
cost and financial burden to the patient
families and health system of any country.
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9. Epidemiology
• Only 3% people with CKD experiences kidney
failure.
• It has been estimated that at least 6% of the
adult population in united states has CKD at
stages 1 and 2.
• An additional 4.5% of us population is
estimated to have stages 3 and 4 CKD,
cumulatively accounting for >90% of the CKD
disease burden worldwide.
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10. Risk factors
• Small for gestational
birth weight
• Childhood obesity
• Hypertension
• Diabetes mellitus
• Autoimmune disease
• Advanced age
• African ancestry
• A family history of -
kidney disease
• A previous history of
acute kidney injury
• Presence of proteinuria
• Abnormal urinary
sediments
• Structural abnormalities
of urinary tract
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11. Etiology
1. Diabetic nephropathy
2. Glomerulo-nephritis
3. Hypertension associated with CKD(includes vascular
and ischemic kidney disease and primary glomerular
disease with associated hypertension)
4. Autosomal dominant polycystic kidney disease
5. Other cystic and tubulo-interstitial nephropathy
6. Systemic inflammatory diseases(SLE, vasculitis)
7. Reno-vascular disease(mostly atheromatous)
8. Congenital (polycystic kidney disease, Alport’s
syndrome)
9. Unknown
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12. Pathophysiology
• It involves two broad sets of mechanism of
damage:
1)Initiating mechanisms specific to the
underlying etiology( e.g. abnormalities in kidney
development or integrity, immune-complex
deposition and inflammation in certain types of
glomerulonephritis, or toxin exposure in certain
diseases of the renal tubules and interstitium).
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13. 2)Hyper-filtration and hypertrophy of the remaining
viable nephrons, that are a common consequence
following long-term reduction of renal mass, irrespective
of underlying etiology and lead to further decline in
kidney function.
• This response to reduction in nephron number are
mediated by vasoactive hormones, cytokines and
growth factors.
• Eventually these shorterm adaptations of hyper
filtration and hypertrophy to maintain GFR become
maladaptive as the increased pressure and flow within
the nephron predisposes to distortion of glomerular
architecture, abnormal podocytes function and
disruption of the filtration barrier leading to sclerosis
and dropout of the remaining nephrons.
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14. Contd..
• Increased intra-renal activity of the RAS
appears to contribute both to the initial
compensatory hyper-filtration and to the
subsequent maladaptive hypertrophy and
sclerosis.
• This process explains why a reduction in renal
mass from an isolated insult may lead to a
progressive decline in renal function over
many years.
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15. Clinical features
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16. Clinical and laboratory manifestations
of CKD and uremia
Fluid , electrolytes and acid base disorders
Sodium and water homeostasis
Potassium homeostasis
Metabolic homeostasis
Disorders of calcium and phosphate metabolism
Cardiovascular abnormalities
Ischemic vascular disease
Heart failure
Hypertension and left ventricular hypertrophy
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18. Contd..
Neuromuscular abnormalities
Gastrointestinal and nutritional abnormalities
Endocrine metabolic disturbances
Dermatologic abnormalities
Hematological abnormalities
Anemia
Abnormal hemostasis
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20. Investigations
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21. Contd..
• Serum and urine protein electrophoresis looking for
multiple myeloma should be obtained in all patients
more than 35years with unexplained CKD, especially if
there associated anemia and elevated or even
inappropriate normal , serum calcium concentration in
the face of renal insufficiency.
• Serum calcium phosphorous , vitamin D and PTh
measured to evaluate metabolic bone disease.
• Hemoglobin concentration, iron , vitamin B 12 and
folate .
• 24 hour urinary protein.
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22. Contd..
• USG (bilaterally small sized kidney exception
are diabetic nephropathy, amyloidosis and HIV
nephropathy)
• PCKD (enlarged kidney with multiple cysts)
• Kidney biopsy not advised in patients with
bilaterally small kidneys
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25. Management
• Initial approach
• History-
– does the patient really have CKD?
– Evidence of chronicity that is more than 3 months, is there a
previous creatinine record?
• Possible causes –
– Ask about history of UTI, LUTS,PMH of hypertension, DM,
IHD, Systemic disorder, renal colic , abnormal urinalysis ,pre-
eclamsia or early pregnancy loss.
• Drug history(NSAIDs , cox-2 inhibitors, antimicrobials,
chemotherapeutic agents, antiretroviral agents , PPIs,
phosphate containing bowel catharteics and lithium.
• Family history( including renal disease and SAH )
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26. Contd..
• Ask about eyes skin and joints.
• Current status-patient may have symptomatic CKD if
GFR less than 30 , symptoms of fluid overload ( Sob,
peripheral edema), uremic syndrome, loss of appetite,
weight loss, nausea, hiccups, peripheral edema, muscle
cramps, pruritus, restless leg, bone pain , amenorrhea ,
impotence, fatigue .
• Examination-
– periphery (peripheral edema, signs of peripheral vascular
disease or neuropathy , vasculitis rash, gouty tophy, joint
disease , avf fistuLA, signs of immunosuppression(bruising
from steroids , skin malignancy ) . Uremic
flap/encephalopathy if GFR less than 15.
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27. Contd..
• Face – anemia , xanthelasma, yellow ting(uremia),
jaundice (hepatorenal ),gum hypertrophy (ciclosporin),
cushingoid (steroids), periorbital edema (nephrotic
syndrome), taut skin /telangiectasia(scleroderma),facial
lipodystrophy(glomerulonephritis)
• Neck- JVP , tunnelled line, scar from
parathyroidectomy, lymphadenopathy.
• CVS – BP, sternotomy , cardiomegaly, signs of
endocarditis, TR if right sided heart failure
• Respiratory- pulmonary edema or effusion
• Abdomen- PD catheter or scars from previous catheter
,signs of previous transplant, ballotable polycystic
kidney or palpable liver .
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28. Treatment
• The aim of management in CKD are to
1. Monitor renal function/appropriate referral to
nephrology
2. Prevent or slow progression of CKD
3. Limit complications of renal failure
4. Treat risk factors for cardiovascular disease
5. Preparation for renal replacement therapy
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29. Monitor renal function/appropriate
referral to nephrology
• GFR and albuminuria should be monitored.
• Drop in eGFR stage with decrease eGFR more
than or equals to 25% is significant.
• Rapid progression is decreased eGFR > 5per
year.
• Every 6 months in patients with stage 3 CKD
but more rapidly or have stage 4 or 5 CKD.
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31. Prevent or slow progression of CKD
• Antihypertensive therapy (reducing
intraglomerular hypertension)
• ACE inhibitors and ARBs are effective in slowing
the progression(both in diabetic and non diabetic
CKD)
• SECOND LINES ARE CCBs(diltiazem and verapamil)
• Glycemic control of hba1c-7%
• Lifestyle-exercise, healthy weight, and smoking
cessation,salt intake <2g/day
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32. • Blood pressure: 140/90 with ckd and no
albuminuria, 130/80 moderately elevated
albuminuria (ACR3-30mg/mmol),125/75 ckd
and heavy proteinuria (pcr >100mg/mmol or
ACR >70 mg/mmol)
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33. Limit complications of CKD
• Anemia : iv iron therapy and erythropoeitin
stimulating agent if hb<11.
• Acidosis: consider it for eGFR<30 and low
serum bicarbonate <20.sodium bicarbonate
supplements ( 1 gm 8 hourly, increasing as
required.
• Oedema: restrict fluid and sodium intake,high
dose loop diuretics.combination of loop and
thiazide diuretics powerful effect.
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34. • Ckd bone mineral disorders: ckd causes
increase in phosphate and reduced
hydrocylation of vit dby kidney. Measure
calcium, phosphate, ALP,PTH and 25-oh vitd if
eGFR<30. treat if phosphate >1.5mmol/lwith
dietary restriction and phosphate binders. The
use of vit d supplements( cholecalciferol,
ergocalciferol) if deficeint.if persistently
increasing pth treat with an activated vit d
analogue (1alpha calcidol or calcitriol.)
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35. • Restless legs/cramps: exclude IDA and then
treat with gaabpentin/pregabalin/dopamine
agonists.
• Dietary advice
• Maintenace of fluid and electrolyte balance.
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36. • Treatment of risk factors for cvd:
Atorvastatin 20 mg and higher if eGFR> 30 for
primary and secondary prevention of cvd.
Antiplatelets(low dose aspirin) for ckd at risk for
atherosclerotic events unless bleeding risk
outweighs benefit.
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37. Preparation for RRT
• Temporary relief of symptoms signs of impending
uremia such as anorexia, nausea, vomitting, lassitude,
and pruritus may sometimes be achieved with dietary
protein restriction.
• Clear indications of RRT for patients with CKD include
uremic pericarditis, encephalopathy, intractable muscle
cramping,anorexia and nausea not atrributable to
reveersibel causes such as PUD, evidence of
malnutrition and fluid and electrolyte abnormalities,
principally hyperkalemia or ECFV overload, that are
refractory to other measures.
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38. • Recommendations for optimal timing for
initiation of RRT
• Patient education
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39. REFERRENCES
• DAVIDSON’S PRINCIPLES AND PRACTICE OF
MEDICINE 22ND EDITION
• HARRISON’S PRINCIPLES OF INTERNAL
MEDICINE 20TH EDITION
• OXFORD HANDBOOK OF CLINICAL MEDICINE.
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40. Thank-you!!!
6/30/2020 BY_ Dr. Anjani k. Jha 40