A slide on Chronic kidney disease. At the beginning of the presentation is a case study, a patient admitted and treated for chronic kidney disease. Other parts covered include relevant anatomy and physiology, aetiopathogenesis and pathophysiology of the condition, as well as management and prevention.

1. MANAGEMENT
OF
CHRONIC KIDNEY DISEASE
BY
Dr. Ernest Osemudiamen Salami,
Department of Internal Medicine,
Central Hospital,
Benin City.

2. OUTLINE
 Introduction
 Relevant Functional Anatomy of the Kidneys
 Definition
 Staging
 Epidemiology
 Aetiology
 Pathogenesis
 Pathophysiology
 Clinical Approach
 History
 Physical Examination
 Investigations
 Treatment
 Dialysis
 Conclusion

3. CASE PRSENTATION
 He is Mr. A.M., a 43 year old storekeeper who resides
at 14, Idemudia street, off Siluko road. He is Muslim
and Eggon.
 Presented with C/O – Bilateral leg swelling x 1/52
– Epigastric pain x 3/7
 He was in his usual state of health until 1 week prior
to presentation when he noticed his legs were
swollen. It was gradual in onset, and progressively
worsened to involve the knees. There are no known
aggravating or relieving factors, and no swelling in
any other part of the body

4.  There is no history of cough, difficulty with
breathing, orthopnoea, PND or easy fatigability
 There is no history of abdominal swelling or
yellowness of the eyes, his HBV and HCV statuses
are unknown, but there is no history of
indiscriminate use of sharps, blood transfusion or
multiple sexual partners. He does not drink alcohol
 There is no history of facial puffiness or reduced
urinary output. There is however, a history of urine
frothiness. He is a known hypertensive diagnosed 7
years ago, not compliant with medications, and
unable to specify the medications.

5.  He is not a known diabetic and his RVD status is not
known. He does not use mercury – containing creams
and soaps, and does not ingest herbal concortions.
 3 days prior to presentation, he developed epigastric
pain, which was sudden in onset, burning and radiating
to the back. Pain is aggravated with hunger and relieved
by meals. Severity of pain was described as 8 using a
scale of 0 – 10.
 There is no associated anorexia, nausea, vomiting,
diarrhoea, melaena stools or haematochezia.
 There is no history of intake of NSAIDs prior to onset of
pain. He is however a suspected PUD patient with
previous episodes of dyspepesia

6.  Following onset of symptom, he presented to a
private facility where he was evaluated and placed
on drugs, whose names he could not ascertain.
PCV done was 19%
 Due to persistence of symptoms, he presented to
this facility for care
 Asthma0, Seizure disorder0, SCA0
Nil hospital admissions nor surgical operations in the
past
 He is married in a monogamous setting with 6
children. He does not smoke or drink alcohol.
 ROS – non-contributory

7.  O/E – a middle-aged man, not in any obvious distress,
pale++, anicteric, acyanosed, not dehydrated, no PLNE,
bilateral pitting pedal oedema up to the knees
 CNS
 Conscious and alert
 Well oriented in time, place and person
 Pupils equal and bilaterally reactive to light
 Power, tone and reflexes all normal
 Nil signs of meningeal irritation
 CVS
 PR – 72 bpm, regular and normal volume
 No thickened arterial wall
 Locomotor brachialis +
 BP – 160/100 mmHg
 JVP – not elevated
 AB – 5th LICS, MCL
 HS – S1, S2 only, nil murmurs heard

8.  RESP
 RR – 18cpm, not dyspnoeic
 Trachea – central
 Symmetrical chest wall movements
 PN – resonant with normal areas of cardiac and hepatic
dullness
 BS – vesicular, nil added sounds
 ABDOMEN
 Full, MWR
 Tenderness ++ at epigastric region
 L0 S0 K0
 BS – heard and normoactive

9.  ASS: CKD 2o hypertensive nephrosclerosis in a
suspected PUD px
 PLAN
 Urgent PCV (22%), E/U/Cr, urinalysis, FSLP
 IV Furosemide 40 mg 12 hourly
 IV Rabeprazole 20mg 12 hourly
 Tab Pilorem–HCT 1 daily
 Tab Spironolactone 25 mg daily

10. 2 – 3 DOA
 Patient seen
 Nil fresh complaints
 Urinalysis
 Colour – amber clear
 Appearance – turbid
 pH – 5.0
 Protein – positive (++)
 Others – normal
 E/U/Cr
 Na – 120 (135 – 150)
 K – 4.0 (3.5 – 5.0)
 Cl – 94 (98 – 108)
 HCO3 – 18 (21 – 28)
 Urea – 174 (10 – 50)
 Cr – 29.3 (0.5 – 1.4)

11.  FSLP
 Cholesterol – 157 (0 – 200)
 TG – 76 (0 – 200)
 HDL – 74 (35 – 80)
 LDL – 68 (50 – 156)
 FBC
 Hb – 7.6 g/dl
 PCV – 22%
 Total WBC – 4600/mm3
 Neutrophil – 64%
 Lymphocyte – 36%
 Monocyte, eosinophil, basophil – nil

12.  O/E – afebrile, pale, anicteric, acyanosed, not
dehydrated, bilateral pedal oedema up to the knees
 PR – 80 bpm, regular, normal volume
 RR – 18cpm
 BP – 170/80mmHg
 ASS: Same
 PLAN
 Renal USS, RVS, HBsAg, HCV
 Transfuse with at least 2 units of whole blood
 IV Torsemide 40mg 12hourly
 D/C IV Furosemide
 Ct other mgt

13. 4 – 6DOA
 Patient seen
 Nil fresh complaints
 Renal USS – findings suggestive of bilateral acute
renal parenchymal disease
 HBsAg, HCV negative
 RVS result not ready
 Not yet transfused due to financial constraints

14.  O/E – afebrile, pale, anicteric, acyamosed, not
dehydrated, bilateral pedal oedema up to the
proximal one – third of the leg
 PR – 64 bpm, regular, normal volume
 RR – 14 cpm
 BP – 150/100 mmHg
 ASS: Same
 PLAN
 Ensure RVS
 Encourage transfusion of blood
 Ct other mgt

15. 7 – 9DOA
 Patient seen
 Nil fresh complaint
 RVS – negative
 Still awaiting blood transfusion
 O/E – afrebile, pale, anicteric, acyanosed, not
dehydrated, bilateral pedal oedema up to the mid
one – third of the legs
 PR – 68 bpm regular, normal volume
 RR – 16 cpm
 BP – 150/100 mmHg

16.  ASS: Same
 PLAN
 Repeat E/U/Cr
 Ct other mgt

17. 10 DOA
 Patient seen
 Nil fresh complaints
 1 unit of blood transfused 3 days ago
 O/E – Afebrile, pale, anicteric, acyanosed, not dehydrated,
bilateral pedal oedema up to the middle one – third of the legs
 PR – 76 bpm, regular, normal volume
 RR – 18 cpm
 BP – 140/90 mmHg
 ASS: Same
 PLAN
 Do post – transfusion PCV
 Tab Rabeprazole 20mg daily
 D/C IV Rabeprazole

18. INTRODUCTION
 CKD implies longstanding (more than 3 months),
and usually progressive, impairment in renal
function.
 In many instances, no effective means are available
to reverse the primary disease process.
 The rate of deterioration in renal function can,
however, be slowed.
 The disease is common in our environment
accompanying conditions such as systemic
hypertension, thereby, justifying this presentation

19. RELEVANT FUNCTIONAL ANATOMY
 The kidneys lie posteriorly in the abdomen,
retroperitoneally on either side of the spine at the
T12–L3 level and are 11–14 cm long.
 The right kidney lies 1.5 cm lower than the left
because of the liver.
 The liver and spleen lie anterior to the kidneys. The
kidneys move downwards during inspiration as the
lungs expand.

21.  Each kidney contains about one million nephrons.
They are the functional units of the kidney
 A nephron consists of a glomerulus, proximal convoluted
tubule, loop of Henle, distal convoluted tubule and
collecting duct, as well as the related vessels.

 Urine is formed by glomerular filtration, modified by
complex processes of secretion and reabsorption in the
tubules, and then enters the calyces and the renal
pelvis.
 The normal GFR is 90 – 120 ml/min/1.73m2

24.  The primary functions of the kidneys are:
 Excretion of waste products of metabolism such as urea
and creatinine
 Maintaining salt, water and electrolyte homeostasis
 Maintenance of acid – base balance
 Regulating blood pressure via the renin–angiotensin
aldosterone system
 Endocrine functions related to erythropoiesis and
vitamin D metabolism.

25. DEFINITION
 The KDIGO 2012 Clinical Practice Guideline for the
Evaluation and Management of Chronic Kidney Disease
defines CKD as either;
 Kidney damage for ≥ 3 months as defined by structural and
functional abnormalities of the kidney manifested by either
pathologic abnormalities, or abnormalities in the composition
of blood and urine, or abnormalities in imaging studies, or a
history of kidney transplantation
OR
 Glomerular filtration rate (GFR) of < 60ml/min/1.73m2 for ≥ 3
months

26. KDOQI STAGING OF CKD
Stage Definition Description Clinical Presentation
1 Kidney damage with
normal or high GFR (>
90)
Mild CKD Asymptomatic
2 Kidney damage and GFR
60–89
Asymptomatic
3A GFR 45–59 Moderate CKD Usually asymptomatic
3B GFR 30–44 Anaemia in some patients at 3B.
Most are non-progressive or
progress very slowly
4 GFR 15–29 Severe CKD First symptoms often at GFR <
20.
Electrolyte problems likely as
GFR falls.
5 GFR < 15 or on dialysis Kidney failure
(End-stage
renal disease)
Significant symptoms and
complications usually present.
Dialysis initiation varies but
usually at GFR < 10

27. EPIDEMIOLOGY
 According to the Global Burden of Disease (GBD), the
global prevalence of CKD was 9.1% (697.5 million
cases) in 2017
 In the same year, CKD resulted in 1.2 million deaths,
and was the 12th leading cause of death worldwide
 CKD is commoner with advancing age groups, in
males than in females, and with co-morbidities such
as diabetes mellitus and hypertension
 In a 2011 study done to assess the prevalence of CKD
amongst adults in a rural population in Edo state, the
prevalence was found to be 27.2%

28.  Over 2 million people worldwide currently receive
treatment with dialysis or renal transplant, yet this
number may represent only 10% of individuals who
actually need treatment to live
 80% of these 2 million are resident in the affluent
nations of the world.
 This therefore means that most of the cases of
ESRD in developing countries cannot access renal
replacement therapy, due to financial hurdles, and
this is a major cause of increased mortality from
CKD in the tropics

29. AETIOLOGY
 The commonest culprits of CKD in this environment include
diabetes mellitus, hypertension, chronic glomerulonephritis, toxic
chemical substances, HIV, HBV, HCV
 Congenital and inherited disease
 Polycystic kidney disease (adult and infantile forms)
 Medullary cystic disease
 Tuberous sclerosis
 Congenital obstructive uropathy
 Glomerular disease
 Primary glomerulonephritides including focal glomerulosclerosis
 Secondary glomerular disease
 Diabetic glomerulosclerosis,
 Accelerated hypertension,
 Sickle cell disease,
 Others include haemolytic uraemic syndrome, thrombotic
thrombocytopenic purpura, systemic sclerosis, systemic lupus,
polyangiitis, Wegener’s granulomatosis, amyloidosis, )

30.  Vascular disease
 Hypertensive nephrosclerosis (common in black
Africans)
 Renovascular disease
 Small and medium-sized vessel vasculitis
 Tubulointerstitial disease
 Tubulointerstitial nephritis – idiopathic, due to drugs
(especially nephrotoxic analgesics), immunologically
mediated
 Reflux nephropathy
 Tuberculosis
 Schistosomiasis

31.  Nephrocalcinosis
 Multiple myeloma (myeloma kidney)
 Balkan nephropathy
 Renal papillary necrosis (diabetes, sickle cell disease
and trait, analgesic nephropathy)
 Chinese herb nephropathy
 Urinary tract obstruction
 Calculus disease
 Prostatic disease
 Pelvic tumours
 Retroperitoneal fibrosis
 Schistosomiasis

32. PATHOGENESIS

33. PATHOPHYSIOLOGY
 As renal function deteriorates with progressive
decline in GFR, systemic complications ensue
 A rough correlation exists between urea and
creatinine concentrations and symptoms.
 These substances are, however, in themselves not
particularly toxic.
 The nature of the metabolites that are involved in
the genesis of symptoms is unclear

34.  The pathophysiological abnormalities in CKD
include;
 Fluid and electrolyte imbalance
 Acid – base imbalance
 Anaemia
 Renal osteodystrophy
 Cardiovascular complications
 Neurological complications
 Gastrointestinal complications
 Endocrine complications
 Immunological disturbances

35. FLUID & ELECTROLYTE
DISTURBANCES
 Fluid and electrolyte balance is maintained until greater than
75% of renal function is lost
 Hypernatraemia – this is due to activation of the RAAS
pathway
 However, in obstructive uropathy and renal dysplasia,
hyponatraemia may occur due to defective urinary
concentrating ability
 Hyperkalaemia usually only occurs at
GFR of < 15 ml/min/1.73m2
 However, in obstructive uropathy, renal dysplasia, reflux
nephropathy and interstitial nephritis may develop
hyperkalaemia at higher levels of GFR due to tubular
resistance to aldosterone.

36. ACID – BASE IMBALANCE
 This occurs early in the disease, when more than
50% of the normal GFR is lost.
 As renal function declines, there is increased
production of ammonium by the remaining
nephrons, and this preserves acid excretion.
 However, with further renal function deterioration,
depression of serum bicarbonate reabsorption
occurs (mainly) in the proximal convoluted tubules.
 Bicarbonate is therefore lost in urine leading to
acidosis.
 It is important to note that metabolic acidosis
impairs phosphate excretion.

38. ANAEMIA
Causes of Anaemia in CKD
 Erythropoietin deficiency (the most significant)
 Bone marrow suppression due to
 Toxins retained in CKD
 Bone marrow fibrosis secondary to
hyperparathyroidism
 Haematinic deficiency – iron, vitamin B12, folate
 Reduced dietary intake
 Altered absorption (iron and hepcidin interplay).

39.  Increased red-cell destruction (reduced survival) due to:
 Abnormal red-cell membranes causing increased osmotic fragility
 Haemodialysis (mechanical, oxidant and thermal damage)
 Increased blood loss:
 Occult gastrointestinal bleeding
 Blood sampling
 Blood loss during haemodialysis
 Platelet dysfunction
 ACE inhibitors (may cause anaemia in CKD, probably by interfering
with the control of endogenous erythropoietin release).
 Decreased GFR and RAAS activation can cause increased plasma
volume at the extent of RBC mass
 Hypothyroidism – reduces GFR and increases PVR
 Aluminium toxicity – from dialysis

42. RENAL OSTEODYSTROPHY

43. CARDIOVASCULAR COMPLICATIONS
The mechanisms involved in uraemic heart disease
include;
 Left ventricular hypertrophy due to
 Fluid overload from salt and water retention
 Systemic hypertension from increased renin production
secondary to reduced blood flow
 Vascular injury from
 Atherosclerosis
 Vascular calcification
 Uraemia per se, causing pericarditis and a
tamponade
 Electrolytes derangement e.g. hyperkalaemia,
hypocalcaemia

44. NEUROLOGICAL COMPLICATIONS
CKD – ASSOCIATED PRURITUS (CKD-aP)
There are theories that attempt to explain the pathophysiology of
CKD-aP
TOXIN DEPOSITION THEORY
 Retention of nitrogenous waste products of protein catabolism.
 Hypercalcaemia
 Hyperphosphataemia
 Elevated calcium × phosphate product
 Hyperparathyroidism (even if calcium and phosphate levels are
normal)
 Iron deficiency.
 Inadequate dialysis (however, a significant number of dialysis
patients who are well dialysed and in whom other causes of
pruritus can be excluded suffer persistent itching, the cause is
unknown)

45. PERIPHERAL NEUROPATHY
 Neuropathic itching is thought to result when
diseased primary afferent sensory neurons or
diseased interneurons are activated out of
proportion to or independent of any pruritogens.
 The fact that patients with paresthesia and restless
leg syndrome more frequently have CKD-aP
supports this theory

46. IMMUNE SYSTEM DYSREGULATION
 This theory of CKD-aP suggests that
microinflammation in the skin and possibly
systemic inflammation stimulate itching.
 Higher levels of inflammatory markers are seen in
dialysis patients, including T-helper 1 cells, C-
reactive protein, interleukin-6, and interleukin-2
 Furthermore, CKD-aP is associated with high white
blood cell counts, low albumin and high ferritin
levels which all point to a dysregulated immune
system

47. OPIOID IMBALANCE
This theory of CKD-aP suggests any of the following
opioid imbalances as culprits;
 Overstimulation of central mu-opioid receptors
 Antagonism of peripheral kappa-opioid receptors
 An imbalance of stimulation and antagonism of mu-
and kappa-opioid receptors

48.  Other neurological manifestations of CKD include
 Uraemic encephalopathy: the exact mechanism is
unknown
 Dialysis dementia
 Restless leg syndrome
 Burning feet syndrome
 Loss of vibration, position, touch and pain sensations
 Carpal tunnel syndrome

49. GASTROINTESTINAL
COMPLICATIONS
These include
 Decreased gastric emptying
 Reflux oesophagitis
 Peptic ulceration
 Acute pancreatitis
 Constipation

50. METABOLIC COMPLICATIONS
 Gout. Urate retention is a common feature of CKD.
 Insulin.
 Insulin is catabolized by and to some extent excreted via the
kidneys. For this reason, insulin requirements in diabetic
patients decrease as CKD progresses.
 By contrast, end-organ resistance to insulin is a feature of
advanced CKD resulting in modestly impaired glucose
tolerance.
 Insulin resistance may contribute to hypertension and lipid
abnormalities.
 Lipid metabolism abnormalities.
 Impaired clearance of triglyceride-rich particles
 Hypercholesterolaemia (particularly in advanced CKD).

51. CLINICAL APPROACH TO A CKD
PATIENT
HISTORY
Particular attention should be paid to:
 Duration of symptoms
 Drug ingestion, including non-steroidal antiinflammatory
agents, analgesic and other medications and
unorthodox treatments such as herbal remedies
 Exposure to nephrotoxic chemical agents in creams and
soaps
 Previous medical and surgical history, e.g. hypertension,
diabetes mellitus, HIV, HBV, HCV, SCD, lower urinary
tract symptoms
 Family history of renal disease
 Exclude the possibility of other differential diagnoses

52.  The early stages of CKD are often completely
asymptomatic, despite the accumulation of
numerous metabolites.
 Symptoms are common when the serum urea
concentration exceeds 40 mmol/L, but many
patients develop uraemic symptoms at lower levels
of serum urea.
 Symptoms include:
 Malaise, loss of energy
 Loss of appetite
 Insomnia

53.  Nocturia and polyuria due to impaired concentrating
ability
 Itching
 Nausea, vomiting and diarrhoea
 Paraesthesiae due to polyneuropathy
 ‘Restless legs’ syndrome (overwhelming need to
frequently alter position of lower limbs)
 Bone pain due to metabolic bone disease
 Paraesthesiae and tetany due to hypocalcaemia

54.  Symptoms due to salt and water retention – peripheral or
pulmonary oedema
 Symptoms due to anaemia
 Amenorrhoea in women; erectile dysfunction in men.
 In more advanced uraemia CKD stage 5, the above
symptoms become more severe and CNS symptoms
are common:
 Mental slowing, clouding of consciousness and seizures
 Myoclonic twitching.
 Severe depression of glomerular filtration can result in
oliguria. This can occur with either acute kidney injury or in
the terminal stages of CKD.
 However, even if the GFR is profoundly depressed, failure of
tubular reabsorption may lead to very high urine volumes; the
urine output is therefore not a useful guide to renal function.

55. EXAMINATION
 Findings on general examination may include:
 Short stature (in patients who have had CKD in
childhood)
 Pallor (due to anaemia)
 Facial puffiness
 Increased photosensitive pigmentation (which may
make the patient look misleadingly healthy)
 Brown discoloration of the nails
 Scratch marks due to uraemic pruritus
 Pedal oedema
 CNS
 Altered consciousness or disorientation in uraemic
encephalopathy
 Glove and stocking peripheral sensory loss (rare)

56.  CVS
 Features of longstanding hypertension
 BP – may be elevated
 JVP – may be elevated
 Pericardial friction rub
 Flow murmurs (mitral regurgitation due to mitral annular
calcification; aortic and pulmonary regurgitant murmurs due to
volume overload)
 Abdominal examination
 Epigastric tenderness in uraemic gastritis
 The kidneys themselves are usually impalpable unless
grossly enlarged as a result of polycystic disease, obstruction
or tumour.
 Rectal examination may disclose enlarged prostate
 Genitourinary examination may reveal an obstruction

58. INVESTIGATIONS
 The main aims for investigations include:
 Identification of the underlying cause where possible,
since this may influence the treatment
 Identification of reversible factors that may worsen renal
function, such as urinary tract obstruction, and salt and
water depletion, electrolytes abnormalities
 Screening for complications of CKD, such as anaemia
and renal osteodystrophy
 Screening for cardiovascular risk factors.

59.  Urinalysis
 Haematuria may indicate glomerulonephritis
 Proteinuria, if heavy, is strongly suggestive of
glomerular disease
 Glycosuria with normal blood glucose is common in
CKD.
 SG may be reduced
 Urine culture, including early-morning urine
samples for TB.
 Urine microscopy
 White cells in the urine usually indicate active bacterial
urinary infection, but this is an uncommon cause of
CKD;
 Sterile pyuria suggests papillary necrosis or renal
tuberculosis.

60.  Eosinophiluria
 Allergic tubulointerstitial nephritis
 Cholesterol embolization.
 Casts.
 Granular casts are formed from abnormal cells within
the tubular lumen, and indicate active renal disease.
 Red-cell casts are highly suggestive of
glomerulonephritis.
 Red cells in the urine may be from anywhere
between the glomerulus and the urethral meatus
 Serum biochemistry
 Urea and creatinine.
 Calculation of eGFR.

61.  Haematology
 Eosinophilia suggests
 vasculitis,
 allergic tubulointerstitial nephritis, or
 cholesterol embolism.
 Markedly raised viscosity or ESR suggests
 myeloma or
 vasculitis.
 Fragmented red cells and/or thrombocytopenia
suggest intravascular haemolysis due to
 accelerated hypertension,
 haemolytic uraemic syndrome or
 thrombotic thrombocytopenic purpura.
 Tests for sickle cell disease should be performed
when relevant.

62.  Immunology
 Complement components may be low in active renal disease due
to SLE, mesangiocapillary glomerulonephritis, post-streptococcal
glomerulonephritis, and cryoglobulinaemia.
 Autoantibody screening is useful in detection of autoimmune
conditions such as SLE , scleroderma Wegener’s
granulomatosis, etc
 Antibodies to streptococcal antigens (antistreptolysin O titre
(ASOT), anti-DNAse B) if post-streptococcal glomerulonephritis is
possible.
 Antibodies to hepatitis B and C may point to
 polyarteritis or membranous nephropathy (hepatitis B) or
 cryoglobulinaemic renal disease (hepatitis C).
 Antibodies to HIV raise the possibility of HIV-associated
nephropathy (HIVAN)

63.  Radiological investigation
 Ultrasound. Every patient should undergo
ultrasonography (for renal size and to exclude
hydronephrosis),
 plain abdominal radiography and CT (without contrast)
to exclude low-density renal stones or nephrocalcinosis,
which may be missed on ultrasound.
 CT is also useful for the diagnosis of retroperitoneal
fibrosis and some other causes of urinary obstruction,
and may also demonstrate cortical scarring.

64.  MRI. Magnetic resonance angiography in renovascular
disease
 Renal biopsy: This should be performed in every person
with unexplained CKD and normal-sized kidneys,
unless there are strong contraindications.
 If rapidly progressive glomerulonephritis is possible, this
investigation must be performed within 24 h of
presentation if at all possible.

66. GFR ESTIMATION

67. TREATMENT
The principles of of management in CKD are:
 Prevention or slowing down of further renal damage
(renoprotection)
 Amelioration of the adverse physiological effects of
renal impairment on the skeleton and on
haematopoiesis
 Treatment of risk factors for cardiovascular disease.
 Preparation for RRT, if appropriate

68. RENOPROTECTION
Antihypertensive therapy
This helps to reduce proteinuria and also reduces the
risk of hypertensive heart failure, stroke and peripheral vascular
disease
In patients with chronic kidney disease, the
recommendations are:
 ACE inhibitor increasing to maximum dose
 Add angiotensin receptor antagonist if goals are not achieved
 Add diuretic to prevent hyperkalaemia and help to control BP
 Add calcium-channel blocker (verapamil or diltiazem) if goals
not achieved
The recommended target BP for CKD treatment is
<120/80mmHg.

69. Reduction of proteinuria
 There is a clear relationship between the degree of
proteinuria and the rate of progression of renal
disease.
 There is strong evidence that reducing proteinuria
reduces the risk of progression.
 Angiotensin-converting enzyme (ACE) inhibitors
and angiotensin II receptor blockers (ARBs) reduce
proteinuria and retard the progression of CKD

70.  Accordingly, ACE inhibitors and/or ARBs should be
prescribed to all patients with diabetic nephropathy
and those with proteinuria, irrespective of whether
or not hypertension is present, providing that
hyperkalaemia does not occur.

71. Dietary/Lifestyle Modifications
 All patients with stage 4 and 5 CKD should be given
dietetic advice aimed at:
 Preventing excessive consumption of protein,
 Ensuring adequate calorific intake
 Limiting potassium and phosphate intake. Dietary
restriction of phosphate is seldom effective alone,
because so many foods contain it.
 Severe protein restriction is not recommended.
 All patients should be advised to stop smoking,
since there is evidence that this slows the
decline in renal function in addition to reducing
cardiovascular risk.
 Exercise and weight loss may also reduce
proteinuria and have beneficial effects on
cardiovascular risk profile.

72. Lipid-lowering therapy
 LDL cholesterol may be normal in CKD but HDL
cholesterol is reduced. Also TGs are elevated
usually
 There is evidence that statins therapy may slow
progression of CKD

73. Maintaining fluid and electrolyte balance
 Fluid retention
 Limitation of daily sodium intake to 100 mmol/day
 Loop diuretics
 Hyperkalaemia
 Reduce or stop potassium-sparing diuretics, ACE
inhibitors and ARBs
 Correct acidosis
 Limiting potassium intake to about 70 mmol/day may be
necessary in late CKD
 Potassium-binding resins, such as calcium resonium,
may be useful in the short term but should not be used
chronically.

74.  The plasma bicarbonate should be maintained
above 22 mmol/L by giving sodium bicarbonate
supplements (starting dose of 1 g 3 times daily,
increasing as required).
 If the increased sodium intake induces
hypertension or oedema, calcium carbonate (up
to 3 g daily) may be used as an alternative, since
this has the advantage of also binding dietary
phosphate.

75. Treatment of Anaemia
 Recombinant human erythropoietin is effective in
correcting the anaemia of CKD and improving the
associated morbidity
 The target haemoglobin is usually between10–20 g/dL.
 Erythropoietin treatment does not influence mortality,
however, and correcting haemoglobin to normal levels
may carry some extra risk, including hypertension and
thrombosis
 Correction of iron deficiency

76. Renal bone disease
 Hypocalcaemia or serum PTH levels more than twice the
upper limit of normal – active vitamin D metabolites (either 1-
α-hydroxyvitamin D or 1,25-dihydroxyvitamin D)
Aim: to reduce PTH levels to between 2 and 4 times the
upper limit of normal
 Hyperphosphataemia
 Dietary restriction of foods with high phosphate
content (milk, cheese, eggs and protein-rich foods)
 Use of phosphate-binding drugs e.g. calcium
carbonate, aluminium hydroxide, lanthanum
carbonate and polymer-based phosphate binders
such as sevelamer.
Aim: to maintain serum phosphate values at 1.8 mmol/L
(5.6 mg/dL) or below if possible, but many of these
drugs are difficult to take and compliance may be a
problem

77.  Tertiary hyperparathyroidism
 Parathyroidectomy
 Calcimimetic agents, such as cinacalcet – they bind to
the calcium-sensing receptor and reduce PTH
secretion. They have a place if parathyroidectomy is
unsuccessful or not possible.

78. DIALYSIS
INDICATIONS
Clinical indications
 Uraemic encephalopathy
 Uraemic gastritis
 Uraemic pericarditis
 Intractable fluid overload or pulmonary oedema
 Intractable hypertension
Laboratory indications
 Urea > 30 mmol/L
 Creatinine > 600 пmol/L
 Hyperkalaemia > 6 mmol/L
 Metabolic acidosis HCO3 < 10 mmol/L
 GFR < 15

79. TYPES
 Hemodialysis
 Solute passively diffuses down concentration gradient
 Dialysate (e.g. acetate, bicarbonate) flows countercurrent to
blood flow.
 Urea, creatinine, potassium move from blood to dialysate
 Calcium and bicarbonate move from dialysate to blood
 Hemofiltration
 Uses hydrostatic pressure gradient to induce filtration/
convention of plasma water + solutes across membrane.
 Peritoneal dialysis
 Uses peritonium as a semi permeable membrane.
Extracorporeal mechanisms not needed

80.  Frequency of dialysis: 4 – 5 hour treatment, 2 – 3 times
a week.
 Complications
 Hypotension
 Hypertension in high dialysate sodium
 Acetate intolerance
 Left ventricular hypertrophy
 Cardiac arrhytmias
 Anaphylactic reaction to ethylene oxide
 Air embolism
 Dialysis disequilibrium
 Peritonitis
 Pericatheter infection

81.  Symptoms of inadequate dialysis
 Insomnia
 Itching
 Fatigue
 Restless legs
 Peripheral sensory neuropathy

82. CONCLUSION
 In the case of CKD, prevention or slowed down
progression is better than overt ESRD.
 This is especially in an environment as ours where most
persons diagnosed with ESRD end up dying due to
inability to foot the bills for a renal replacement therapy
 Hence, it cannot be overemphasized, the importance of
catching the disease in the early stages and applying
renoprotection, through profound knowledge of the
subject matter, good clinical acumen and superb clinical
decision making

83. THANK YOU FOR
LISTENING!

84. REFERENCES
 Principles and Practice of Medicine 22e
 Kumar and Clark Clinical Medicine 8e
 Paediatrics and Child Health in Topical Region 3e
 Aug. 2011, Volume 8, No. 8 (Serial No. 81), pp.
471-481 Journal of US-China Medical Science,
ISSN 1548-6648, USA . Prevalence of Chronic
Kidney Disease and Its Risk Factors amongst
Adults in a Rural Population in Edo State, Nigeria;
Ogochukwu Chinedum Alice Okoye, Efosa Oviasu
and Louis Ojogwu
 www.nkf.com
 www.medscape.com