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Chronic Kidney Disease

Chronic renal failure, or chronic kidney disease (CKD), is a progressive decline in kidney function characterized by structural and functional abnormalities, leading to the need for renal replacement therapy. Symptoms can range from asymptomatic to severe manifestations like fatigue, anemia, and cardiovascular issues, with diagnosis involving blood tests, urinalysis, and imaging. Treatment strategies focus on managing blood pressure, diabetes, proteinuria, cardiovascular risks, and may include renal replacement therapy in advanced stages.

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0% found this document useful (0 votes)
9 views16 pages

Chronic Kidney Disease

Chronic renal failure, or chronic kidney disease (CKD), is a progressive decline in kidney function characterized by structural and functional abnormalities, leading to the need for renal replacement therapy. Symptoms can range from asymptomatic to severe manifestations like fatigue, anemia, and cardiovascular issues, with diagnosis involving blood tests, urinalysis, and imaging. Treatment strategies focus on managing blood pressure, diabetes, proteinuria, cardiovascular risks, and may include renal replacement therapy in advanced stages.

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hussainmahid889
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Chronic renal failure

Lecturer: Damirbek Abibillaev


International Ala-Too University
Medical Faculty
Department of Therapeutic Disciplines and Family Medicine
Definition
• Chronic renal failure, also known as chronic kidney disease (CKD), is a
progressive and irreversible decline in kidney function over time.
• It is characterized by structural and functional abnormalities of the
kidneys, leading to the gradual loss of their ability to filter waste
products and regulate fluid and electrolyte balance.
Definition
• Chronic kidney disease (CKD) is defined as the presence of kidney
damage or an estimated glomerular filtration rate (eGFR) less than 60
ml/min/1.73 mt2, persisting for 3 months or more, irrespective of the
cause.
• It is a state of progressive loss of kidney function ultimately resulting
in the need for renal replacement therapy (dialysis or
transplantation).
• Kidney damage refers to pathologic abnormalities either suggested by
imaging studies or renal biopsy, abnormalities in urinary sediment,
or increased urinary albumin excretion rates.
Cause
Examples

Chronic tubulointerstitial nephropathies

Focal segmental glomerulosclerosis


Glomerulopathies (primary)
Idiopathic crescentic glomerulonephritis

Amyloidosis
Glomerulopathies associated with systemic
Diabetes mellitus
disease
Systemic lupus erythematosus

Medullary cystic kidney disease


Hereditary nephropathies
Alport syndrome

Hypertension Hypertensive nephrosclerosis

Benign prostatic hyperplasia


Obstructive uropathy
Posterior urethral valves

Renal macrovascular disease (vasculopathy of Renal artery stenosis caused by atherosclerosis


renal arteries and veins) or fibromuscular dysplasia
Symptoms and signs
• Patients with mildly diminished renal reserve are asymptomatic.
• Even patients with mild to moderate renal insufficiency may have no
symptoms despite elevated blood urea nitrogen (BUN) and creatinine.
• Nocturia is often noted, principally due to failure to concentrate the
urine.
• Lassitude, fatigue, anorexia, and decreased mental acuity often are
the earliest manifestations of uremia.
Symptoms and signs (Neuromauscular)
With more severe renal disease (eg, estimated glomerular filtration
rate [eGFR] < 15 mL/min/1.73 m2), neuromuscular symptoms may be
present:
• coarse muscular twitches
• peripheral sensory and motor neuropathies
• muscle cramps
• Hyperreflexia
• restless legs syndrome
• seizures (usually the result of hypertensive or metabolic
encephalopathy).
Symptoms and signs (constitutional and
dermatologic)
• Anorexia, nausea, vomiting, weight loss, stomatitis, and an
unpleasant taste in the mouth are almost uniformly present.
• The skin may be yellow-brown and/or dry.
• Occasionally, urea from sweat crystallizes on the skin (uremic frost).
• Pruritus may be especially uncomfortable.
• Undernutrition leading to generalized tissue wasting is a prominent
feature of chronic uremia.
Symptoms and signs (Cardiovascular)
• In advanced CKD, pericarditis and gastrointestinal ulceration and
bleeding may occur.
• Hypertension is present in > 80% of patients with advanced CKD and
is usually related to hypervolemia.
• Heart failure caused by hypertension or coronary artery disease and
renal retention of sodium and water may lead to dependent edema
and/or dyspnea.
Diagnosis
• Electrolytes, blood urea nitrogen (BUN), creatinine, phosphate,
calcium, complete blood count (CBC)
• Urinalysis (including urinary sediment examination)
• Quantitative urine protein (24-hour urine protein collection or spot
urine protein to creatinine ratio)
• Ultrasonography
• Renal biopsy
Stages of CKD
• Stage 1: Normal GFR (≥ 90 mL/min/1.73 m2) plus either persistent
albuminuria or known structural or hereditary renal disease
• Stage 2: GFR 60 to 89 mL/min/1.73 m2
• Stage 3a: 45 to 59 mL/min/1.73 m2
• Stage 3b: 30 to 44 mL/min/1.73 m2
• Stage 4: GFR 15 to 29 mL/min/1.73 m2
• Stage 5: GFR < 15 mL/min/1.73 m2
Treatment strategies
• Blood Pressure Control: Strict blood pressure control, typically targeting a goal
blood pressure of <130/80 mmHg, is essential in slowing the progression of CKD
and reducing the risk of cardiovascular events. Renin-angiotensin-aldosterone
system (RAAS) inhibitors (e.g., ACE inhibitors, ARBs) are first-line agents for blood
pressure management in CKD.
• Diabetes and Glycemic Control: Optimal glycemic control is crucial in patients
with diabetes mellitus to delay the progression of CKD and reduce the risk of
diabetic nephropathy. Lifestyle modifications, antihyperglycemic medications,
and regular monitoring of glycemic parameters are essential components of
diabetes management in CKD.
• Proteinuria Management: Reduction of proteinuria with RAAS inhibitors, such as
ACE inhibitors or ARBs, is associated with renoprotective effects and improved
outcomes in CKD. Other antiproteinuric agents, such as mineralocorticoid
receptor antagonists (e.g., spironolactone), may be considered in patients with
persistent proteinuria despite maximal RAAS inhibition.
Treatment strategies
• Cardiovascular Risk Management: Patients with CKD are at increased
risk of cardiovascular disease and require aggressive management of
cardiovascular risk factors, including dyslipidemia, smoking cessation,
and lifestyle modifications.
• Anemia Management: Anemia is common in CKD due to decreased
production of erythropoietin by the kidneys. Treatment may involve
erythropoiesis-stimulating agents (e.g., erythropoietin, darbepoetin),
iron supplementation, and correction of underlying factors
contributing to anemia.
Treatment strategies
• Bone and Mineral Metabolism Management: CKD-mineral and bone
disorder (CKD-MBD) is characterized by abnormalities in calcium,
phosphate, parathyroid hormone (PTH), and vitamin D metabolism.
Treatment aims to maintain serum calcium and phosphate within
target ranges, suppress elevated PTH levels, and optimize vitamin D
status.
• Dietary and Lifestyle Modifications: Dietary modifications, including
sodium restriction, protein restriction (in advanced stages of CKD),
and avoidance of nephrotoxic substances (e.g., NSAIDs, contrast
agents), are essential components of CKD management. Lifestyle
modifications such as regular exercise, smoking cessation, and weight
management are also recommended.
Renal replacement therapy
• In advanced stages of CKD (stage 5 or ESRD), renal replacement
therapy options include hemodialysis, peritoneal dialysis, and kidney
transplantation.
• The choice of RRT modality depends on patient preferences, clinical
status, comorbidities, and resource availability.
Prognosis
• Progression of chronic kidney disease (CKD) is predicted in most cases
by the degree of proteinuria.
• Patients with nephrotic-range proteinuria (> 3 g/24 h or urine
protein/creatinine ratio > 3) usually have a poorer prognosis and
progress to renal failure more rapidly.
• Progression may occur even if the underlying disorder is not active. In
patients with urine protein < 1.5 g/24 h, progression usually occurs
more slowly if at all.
• Hypertension, acidosis, and hyperparathyroidism are associated with
more rapid progression as well.

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