Republic of Iraq
Ministry of Higher Education and Scientific Research
University of Baghdad - College of Medicine
Department of Medicine
Chronic Kidney Disease
Done by Supervised by
Ahmed Ali Hussein Prof. Dr. Waleed Al-Ansary
Sixth grade student
Objectives
Identification of chronic kidney disease (CKD).
Explain the classification of CKD according to KDIGO.
Identify the epidemiology of CKD among people.
Demonstrate the pathophysiology and risk factors of CKD.
Describe clinical manifestations and diagnosis of CKD.
Explain management of CKD and its complications
How to prepare the patient with CKD for RRT.
Introduction (1,2)
Chronic kidney disease is an irreversible deterioration in renal function
that slowly progress over a period of years, Unlike acute kidney damage ,
the kidney damage in CKD is rarely repaired, so loss of function persists.
CKD manifestations range from an abnormalities detectable only by
laboratory testing, to a clinical syndrome known as uraemia.
The severity of CKD is graded by the decreased level of the glomerular
filtration rate (GFR) and albuminuria. (Figure 1)
Green: Low risk (if no other markers of kidney disease, no CKD).
Yellow: Moderately increased risk.
Orange: High risk.
Red: Very high risk.
Figure 1 – Kidney Disease Improving Global Outcome (KDIGO) classification of chronic kidney
disease (CKD) (4)
Epidemiology (2,3)
• The prevalence of CKD stages 3–5 (eGFR < 60 mL/min/1.73 m2) are
around 5–7%.
• The demographic factor most strongly associated with increased risk of
CKD is age, Mostly affecting people aged 65 years and above.
• The higher prevalence of CKD in patients with hypertension, diabetes and
vascular disease.
• More than 25% of the population aged over 75 years have an eGFR of <60
mL/min/1.73 m2, mostly stage 3A CKD.
Pathophysiology (4)
There are two broad sets of mechanisms of damage:
1. Initiating mechanisms specific to the underlying etiology (e.g.,
genetically determined abnormalities in kidney development or
integrity, immune complex deposition and inflammation in certain
types of glomerulonephritis, or toxin exposure)
2. Set of progressive mechanisms, involving hyperfiltration and
hypertrophy of the remaining viable nephrons, that are a common
consequence following long-term reduction of renal mass,
irrespective of underlying etiology. (Figure 2)
Figure 2 – Left: Schema of the normal glomerular architecture. Right: Secondary glomerular changes
associated with a reduction in nephron number, including enlargement of capillary lumens and focal
adhesions, which are thought to occur consequent to compensatory hyperfiltration and hypertrophy in the
remaining nephrons. (4)
Risk Factors (2,4)
Diabetes mellitus.
Drug-induced interstitial disease.
IgA nephropathy.
Hypertension.
Childhood obesity.
Autoimmune disease.
Advanced age.
A family history of kidney disease.
A previous episode of acute kidney injury.
Proteinuria, abnormal urinary sediment.
Structural abnormalities of the urinary tract.
Clinical Manifestations (1–3) (Figure 3)
The typical presentation of CKD is caused by a raised urea and creatinine.
Most patients with slowly progressive disease are asymptomatic.
As the GFR declines, clinical abnormalities become more frequent, and most
patients develop more overt symptoms of uremia, including fatigue,
anorexia, nausea, vomiting, and confusion.
Uremia can also induce serositis, especially pericarditis and tamponade.
Some patients with renal bone disease complain of vague, ill-defined pain in
the lower back, hips, knees, and other locations.
Calciphylaxis is calcification of the skin and cutaneous vessels, often with
resulting pruritus.
Figure 3 – Physical signs in advanced chronic kidney disease. (2)
Diagnosis (1)
If CKD is suspected, emphasis should be placed on eliciting a history of
hypertension, urinary abnormalities, and treatment with drugs that might
affect kidney function (e.g. NSAIDs).
The family history should focus on family members with kidney diseases,
diabetes, hypertension, kidney stones, or surgery involving the urinary tract.
The physical examination should include blood pressure measurements plus
a search for CKD associated findings such as skin abnormalities, persistent
itching, a palpable polycystic kidney, evidence of lost lean body mass, the
presence of peripheral edema, and neurologic abnormalities.
Blood chemistries should include sodium, potassium, chloride, bicarbonate,
calcium, phosphorus, alkaline phosphate, PTH, and uric acid levels.
An elevated serum creatinine and BUN levels and other findings indicating
the presence of CKD include anemia, metabolic acidosis, hyperkalemia,
hyperphosphatemia, hypocalcemia, and hypoalbuminemia. Blood glucose
level and hemoglobinA1c level should be monitored. Measurements of
antinuclear antibody (ANA), double-stranded DNA antibodies, serum
complement and antineutrophil cytoplasmic antibody levels are needed , as
well as an evaluation for hepatitis viruses A, B, and C
Management (2)
• Monitor renal function
• Prevent or slow further renal damage
• Limit complications of renal failure
• Treat risk factors for cardiovascular disease
• Prepare for RRT, if appropriate
• Monitoring renal function every 6 months in patients with stage 3 CKD, but more
frequently in patients who are deteriorating rapidly or have stage 4 or 5 CKD.
• ACE inhibitors or ARBs should be prescribed with caution to all patients with
diabetic nephropathy and patients with CKD and proteinuria, irrespective of
whether or not hypertension is present.
Complications and Management (1,3)
Cardiovascular complications:
• Hypertension: The preferred regimen is an ACE inhibitor or
angiotensin receptor blocker (but never the two together) in
combination with a diuretic
• Dyslipidemia: KDIGO guidelines recommend treatment with statins
for patients over age 50 years with an eGFR <60 mL/min/1.73 m2
and/or albuminuria.
• Coronary Artery Disease: The association increases with lower
levels of eGFR and higher levels of albuminuria. Despite this excess
risk, patients with CKD are paradoxically less likely to be treated for
the prevention of CAD. Moreover, patients with CKD are less likely
to receive coronary revascularization procedures
Chronic Kidney Disease-Mineral and Bone Disorder:
• Vascular calcification: KDIGO guidelines therefore suggest treating
patients with CKD and arterial calcification as is appropriate for
patients in the highest category of cardiovascular risk.
• Renal Osteodystrophy:
• Osteitis Fibrosa Cystica.
• Adynamic Bone Disease.
• Osteomalacia.
• Osteoporosis.
Treat secondary hyperparathyroidism, correct vitamin D deficiency
and normalize the serum calcium and phosphorus. Tertiary
hyperparathyroidism patients often require parathyroidectomy
Anemia:
Oral iron supplements can replete iron stores over a period of 3 to 4
months but are associated with adverse gastrointestinal events. When iron
stores are adequate, anemia should be corrected with erythropoietin.
Metabolic Acidosis:
Occurs due to progressive loss of the ability of the kidneys to regenerate
bicarbonate. KDIGO guidelines now suggest treatment of patients with
CKD with alkali (eg, sodium bicarbonate and sodium citrate) to maintain
serum bicarbonate in the normal range
Figure 4 – Conceptual model for the development, progression, and complication of CKD (5)
Preparation for Renal Replacement Therapy (2,4)
Temporary relief of symptoms and signs of impending uremia, such as anorexia,
nausea, vomiting, and pruritus, may sometimes be achieved with protein restriction.
Maintenance dialysis and kidney transplantation have extended the lives of hundreds
of thousands of patients with CKD worldwide.
Clear indications include uremic pericarditis, encephalopathy, intractable muscle
cramping, anorexia, nausea not attributable to reversible causes, evidence of
malnutrition, and fluid and electrolyte abnormalities, principally hyperkalemia.
Physical preparations include establishment of timely access for hemodialysis or
peritoneal dialysis and vaccination against hepatitis B.
Conclusion
Chronic kidney disease is an irreversible damage of the kidney.
Mostly affecting people aged 65 years and above.
Level of the glomerular filtration rate (GFR) and albuminuria are used
in the grading of the disease.
CKD managed by monitoring renal function, treat the complications
and prevent further damage to the kidney.
Any patient with CKD should be prepared for RRT after temporary
relief symptoms of uremia.
References
1. Goldman L, Schafer AI. Goldman-Cecil Medicine. 26th ed. 2020. 799–804 p.
2. Ralston SH, Penman ID, Strachan MWJ, Hobson RP. Davidson’s Principles and
Practice of Medicine. 23th ed. Elsevier Ltd; 2018. 415–420 p.
3. Masters, Philip A. MD F. Nephrology. In: MKSAP. 17th ed. 2018. p. 75–9.
4. Dennis L. Kasper M, Stephen L. Hauser M, J. Larry Jameson, Md P, Anthony s. Fauci
M, dan L. Longo M, Joseph Loscalzo, Md P. Harrison’s Principles pf Internal
Medicine. 19th ed. McGraw-Hill Education; 2015. 1811–1821 p.
5. Nahas M El, Levin A. Chronic Kidney Disease. Oxford university press; 2009. 84 p.
