CHRONIC KIDNEY DISEASEDR. A.O SHITU

INTRODUCTION

This a condition in which there is kidney tissue damage

manifested by pathologic abnormalities or markers of

damage with or without a reduction in the GFR

persisting for at least 3months

Impaired renal function for >3months based on

abnormal structure or function or GFR

<60ml/min/1.73m2 for >3months with or without

evidence of kidney damage

STAGING OF CKD

ESRD

This terminology is used to describe the clinical condition of chronic renal

disease with the patient requiring renal replacement therapy (dialysis or

transplant)

It is defined as GFR <15ml/min/1.73m2 or need for renal replacement

therapy

It is diagnosed when a patient has a transplant or dialysis for >90days or

dies within 90days after commencing dialysis in the anticipation that he

would require dialysis indefinitely

It excludes patients who are thought to have ESRD and started on RRT but

subsequently recovers within 90days

AETIOLOGY

Chronic glomerulonephritis

Hypertensive disease

Primary essential hypertension

Renovascular occlusive disease

Diabetic nephropathy

Interstitial nephritis

Obstructive uropathy

Polycystic kidney disease

Chronic pyelonephritis

HIVAN

Sickle-cell nephropathy

Amyloid disease

Gout nephropathy

Malignant infiltrative disease

Sequelae to acute kidney injury

Heredofamilial kidney disease e.g Alportsyndrome

Renal stones

PATHOPHYSIOLOGY

Progressive destruction of nephrons with hyperfiltration and

compensatory hypertrophy of the remaining nephrons

This is initially beneficial, but subsequently leads to the progressive

renal dysfunction. The increased glomerular capillary pressure leads to damage of the capillaries and this leads to secondary focal

and segmental glomerulosclerosis and eventually to global

glomerulosclerosis

Subsequently there is dysfunction of the paratubular cells and loss

of the unexcretory function of the kidneys.

FACTORS THAT CAUSE PROGRESSION

Systemic hypertension

Nephrotoxins (NSAIDS, contrast)

Decreased perfusion

Proteinuria

Hyperlipidaemia

Hyperphosphataemia with calcium phosphate deposition

Smoking

Uncontrolled diabetes

CLINICAL APPROACH TO THE PATIENT

WITH CKD

Patients with CKD stages 1-3 are frequently asymptomatic in the terms of possible negative symptoms related simply to the loss of GFR. Thus, they don’t experience overt disturbances in water or electrolyte balance or endocrine/metabolic derangement

These disturbances become clinically evident with CKD stage 4-5 the positive symptoms

Reduction in urine output

Heamturia

Oedema

Patient with tubulointerstitial disease, cystic diseases, nephrotic syndrome the signs show up much earlier

HISTORY

Duration of symptoms

Drug ingestion

Previous medical and surgical history

Pervious occasions

Family history

SYMPTOMS OF NEPHRON DAMAGE

Nocturia and polyuria

Reduced urine output

Oedema

SYMPTOMS OF UREAMIA

Malaise

Anorexia

Insomnia

itching

Nausea, vomiting, and diarrhea

Parasthesia

Restless leg syndrome

SYMPTOMS OF COMPLICATIONS

Symptoms of anaemia

Bone pain

Paresthesia due to hypocalcaemia

Amenorrhoea in women and erectile dysfunction in males

In stage 5 disease

Mental slowing, altered consciousness and seizures

Myoclonic twitching

EXAMINATION

Short stature

Pallor

Brownish discoloration of the nails

Scratch marks

Signs of fluid overload

Evidence of the aetiology

CVS

Signs of pericaridits

Hypertension

Heart failure

CNS

Confusion

Coma

SKIN

Uraemic frost

Epitaxis and bruising

CHEST

Breathlessness

Signs of consolidation

INVESTIGATION

URINALYSIS

Heamaturia

Proteinuria

Urine culture

URINE MICROSCOPY

WBC

RBC

Eosinophilia

Casts – broad waxy casts

URINE BIOCHEMISTRY

Measurement of urinary electrolytes

Not so helpful in CKD

Urine osmolality

Measure the concentrating power of

the kidneys

Urine electrophoresis and

immunofixation

Detection of light chains

HEAMATOLOGY

RBC indices

Fragmented RBC and/or

thrombocytopenia may indicate HTN

and renovascular disease

ESR – roles out vasculitis

Test for sickle cell disease

SERUM BIOCHEMISTRY

U/E/Cr, Ca, PO4, and uric acid

Increased urea and creatinine

Hyperkalemia

Hyperphosphataemia

hypocalcemia

Estimation of eGFR

Cockfort Gault

MDRD

CKD EPI

SEROLOGY

Autoantibody screening

Complement components

Serology for hepatitis B and C virus

RVD screening

RADIOLOGICAL INVESTIGATION

Ultrasound: size, echogenicity and

corticomedullary differenciation

CT : cortical scarring, urinary

obstruction

MRI: renovascular disease

COMPLICATIONS OF CKD

ANAEMIA

Erythropoietin deficiency

Bone marrow toxins

Bone marrow fibrosis

Haematinic deficiency

Increased red-cell destruction

Abnormal red-cell membranes

Increased blood loss

ACE inhibitors

BONE DISEASE: RENAL OSTEODYSTROPHY

Bone mineral disorder which encompasses several disorders : hyperparathyroidbone disease, osteomalacia, osteoporosis, osterosclerosis and adynamic bone disease

Its pathogenesis involves

Phosphate retention

Increased fibroblast growth factor 23

Downregulation of 1alpha hydroxlase and thus reduced 1,25-dihydroxycholecalciferol

hypocalcemia

Increase PTH levels (secondary hyperparathyroidism)

SKIN DISEASE

Pruritus

Eczematous lesions

Porphyria cutanea tarda

Nephrogenic systemic fibrosis

GASTROINTESTINAL

Reflex osteophagitis

Peptic ulceration

Acute pancreatitis

Constipation

Usually seen in patients on CAPD

METABOLIC ABNORMALITIES

Gout from urate retention

Reduces insulin requirement in diabetics

Lipid metabolism abnormalities

Impaired clearance of triglyceride rich proteins

Hypercholesterolaemia

Heparinization in HD and glucose absorption in PD contributes

ENDOCRINE ABNORMALITIES

Hyperprolactinemia

Increased LH levels

Decreased testosterone

Amenorrhoea

Impaired GH action

Reduce thyroid hormone levels

NERVOUS SYSTEM

CNS

Severe ureamia with depressed

cerebral function and seizures

Psychiatric problems

Dialysis associated

Disequilibrium syndrome

Dialysis dementia (aluminium)

PNS

Median nerve compression

Restless leg syndrome

Polyneuropathy

Autonomic nervous system

Increased catecholamine levels

Impaired efferent vagal function

CARDIOVASCULAR DISEASE

Patients with CKD have a 16 fold increase in risk of developing CVD, particularly MI, cardiac failure, sudden cardiac death and stroke

Risk factors include

Hypertension

Dyslipidaemia

Raised calcium x phosphate product

Hyperparathyroidism

Vascular calcification

Inflammation

Hyperhomocysteinaemia

Calciphylaxis

Calcific uraemic arteriopathy, its rare and is a contributory factor to death in

dialysis patients

Presents with painful non-healing eschars with panniculitis and dermal necrosis

Pericarditis

Ureamic pericariditis

Dialysis pericarditis

MANAGEMENT

Management Strategies

Primary-prevention – Prevent modifiable risk factors

Secondary prevention in control HT/DM/GN/UTI/obstructive uropathy

Control/treatment of complications

Correct all potentials reversible factors

Correct mineral/electrolyte abnormalities

Careful dietary control

Prevention of further loss of function

Attempt to retard progression

Attend to drugdosage schedules

Establish level of renal failure

(Function/Structure)

Identify complications: HT/UTI/anaemia/CV/osteodystrophy etc.

Identify nature of underlying renal disease obstructive uropathy SLE etc.

Adequate knowledge of risk factors

for CKD

Adequate Knowledge of early features of CKD

Adopting appropriate Health seeking attitude behavior

Life style changes

Smoking

Alcohol

Exercise

Obesity

Analgesic/Herbal concoctions/Drugs

Prevention of communicable disease environmental sanitation/adequate

control of infective conditions/immunization Hepatitis B & C); HIV control

prevention treatment

Primary healthcare screening

Proteinuria for HT/DM

Management of complications/Retardation of Progression

HT Control: Target BP < 130/80

Drugs Renoprotective – ACEi, ARBs

+ other drugs

Dietary

Protein: 0.6g/kg day (high biological value)

Calories: 3000Kcal/day

Add vits

Reduce saturated fats

Na intake: 40 – 60 mEq/day

K: 20 – 40 mEq/day (in severe cases)

Fluid intake – regulated (previous day urine output + 1-1.2 litre)

Drug dosages – tailored to renal function

Acidosis

Metabolic acidosis with a reduction in net Hydrogen ions secretion occurs

in all forms of CKD.

Malnutrition, reduction of Album synthesis and bone dissolution

Use of NaHCO3 tend to mitigate the impacts

Anaemia

Target 11-12G/dl

Replesnish iron stores

Serum ferritin>100ng/ml,

Treat with Epo and iron (oral or parenteral)

Other adjunctive drugs:-

haematinics

Ca/P04/vit D/PTH

Maintain P04a3.0 – 4.6 mg/dl/

Ca 8.8 – 9.5 mg/dl/

SP ≤55mg2/dl-2

Bind P04

Ca based P04 binders

Non Ca based binders

Restrict dietary P04 to 800 – 1000 mg/d

Vit D analogues

Calciminetics

RENAL REPLACEMENT THERAPY

Reserved mainly for patient with end-stage disease

Peritoneal dialysis

Haemodialysis

Kidney transplantation

Progression of Chronic Kidney Disease and Interventional Strategies

15

30

GFR

60

90

120

CKD1 CKD2 CKD3 CKD4 CKD5

120

110

≤ 89

≤ 59

29

<15

Health But+ At Risk

- Active Cotrol of Uraemia- - treatment of

complications- - (Anaemia/Bone

Disease/CVD and others)

- Low - Early detection protection

- low salt- statins

- Early detection- low protein- low salt

- Renoprotection- CV risk factors- Control(treatment)

- Optimal Control - Attitude/Behaviour- lifestyle- Renoprotective

>90>90

>60

>30

>15