Long term complications of chronic kidney disease

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There are many complications of chronic kidney disease (CKD). When it does not treat correctly, it may increase morbidity and mortality.

Table of Contents

Uremia means urine in the blood. It is a type of blood poisoning resulting from the retention of waste products usually excreted as urine.

Uremia results from the failure of the excretory and endocrine functions of the kidneys.
It is a syndrome that summarizes the main symptoms of end-stage renal failure.
A decrease in the glomerular filtration rate leads to an accumulation of toxic metabolites, which results in the increase of Blood Urea Nitrogen (BUN) and Creatinine in the blood.
The impaired tubular function leads to imbalance in the electrolyte, water and acid-base balance.
The reduced synthesis of erythropoietin and 1.25 OH₂ (vitamin D₃) leads to renal anemia and renal osteopathy respectively.
Uremia can be endogenous poisoning that manifests itself in disorders of the heart, gastrointestinal tract, brain and nerves, blood formation and immune system.
Adequate and regular dialysis is the best method to reduce uremic syndrome.
Causes of uremia are acute and chronic kidney disease.
There are many symptoms like nausea, vomiting, fatigue, anorexia, weight loss, muscle cramps, pruritus, mental status changes and many more
The ultimate treatment of uremia is renal replacement therapy (Dialysis and kidney transplant).
Besides all the preventing measures of kidney disease, regular and adequate dialysis can prevent the uremia

Renal anemia is caused by the kidneys producing too little erythropoietin (EPO) hormone due to a functional deficiency. In simple, anemia in chronic kidney disease (CKD) is called renal anemia.
Erythropoietin (EPO) stimulates the formation of red blood cells in the bone marrow.
Renal anemia can be the result of chronic kidney disease or kidney damage.
The resulting renal anemia usually aggravates by a shortened lifespan of red blood cells.
Managing kidney disease may help to delay or prevent renal anemia from getting worse.
Renal anemia leads to left ventricular hypertrophy; also, myocardial ischemia and cardiac decompensation are possible.
The typical classic symptoms are fatigue, dizziness and shortness of breath. Others are headache, unusual heartbeat, pale and dry skin, chest pain etc.
Causes of renal anemia can be erythropoietin deficiency because of uremic toxins, iron deficiency, shortens Erythrocyte’s survival time, vitamin deficiency – Vit B12 and folic acid, inadequate dialysis etc.
Besides Erythropoietin (EPO) and iron supplementation, red blood cell transfusion can treat renal anemia. Vitamin supplements such as vitamin B12 or folate may need to make healthy blood cells.

Renal osteopathy is a metabolic bone disorder that occurs in chronic renal insufficiency due to secondary hyperparathyroidism, osteomalacia.
Bone metabolism includes phosphate, calcium, vitamin D, Parathyroid hormone.
It results in bone and joint pain, increased bone fragility, and relative muscle weakness for the patient.
The special significance of the disease reflects together with the bone problems; increased arteriosclerosis associated with a high risk of heart attack, stroke and death.
Therapeutic options include the substitution of calcitriol, calcium, calcium carbonate, and as a surgical measure, parathyroidectomy.

There is an increasing tendency to retain hydrogen ions and increase the accumulation of acid equivalents in chronic renal failure.
Less commonly, there is primary renal or extrarenal bicarbonate loss or decreased renal acid excretion.
It results in metabolic acidosis with arterial pH < 7.35 and bicarbonate levels between 12 and 20 mmol/l, rarely < 10 mmol/l.
Metabolic acidosis in CKD should treat as early as possible.
Excess hydrogen ions activate the bone buffer, leading to the release of calcium and phosphate with possible worsening of renal osteopathy.
Acidosis may increase skeletal muscle breakdown and decrease albumin synthesis, resulting in loss of substance and muscle weakness.
In addition, erythrocyte survival shortens in the acidic environment.
Oral intake of sodium bicarbonate is recommended, with a target value for bicarbonate of 22 mmol/l.

Volume and sodium balance usually maintain up to a glomerular filtration rate (GFR) of 10-15 ml/min.
Nevertheless, there is a risk of volume overload even in patients with mild to moderate renal insufficiency.
Limitation of salt intake and use of loop diuretics, if necessary, is recommended.
A decreased ability to excrete sodium in later stages of the disease follows a positive sodium balance with hypertension and oedema.
The result of overhydration are oedema (water retention), hypertension (high blood pressure), left heart failure (left heart failure), pulmonary oedema (water retention in the lungs), cerebral oedema (swelling of the brain)
Serum potassium is normal as long as sufficient aldosterone is available in chronic renal failure and secretion of potassium in the distal tubule is maintained.
Hyperkalemia may occur in oliguric patients as well as high potassium intake, treatment with potassium-sparing diuretics (spironolactone), tissue breakdown, marked metabolic acidosis, or hypoaldosteronism.
ACE inhibitors, AT1 receptor blockers, and nonsteroidal anti-inflammatory drugs (NSAID) promote hyperkalemia.
Treatment is with a low-potassium diet, loop diuretics, compensation of acidosis if necessary, and in emergencies, additional glucose-insulin infusions, ion exchangers, and dialysis.

Common comorbidities and complications include arterial hypertension, left ventricular hypertrophy, coronary artery disease, heart failure, ventricular arrhythmias, accelerated atherosclerosis of the vessels, endocarditis, pericarditis, and strokes.
In dialysis patients, along with the development of arteriosclerosis, there is calcification of the heart valves and middle arterial walls with stiffening of the vessels.
Hyperphosphatemia with accompanying hypercalcemia is thought to be a major cause. For this reason, treatment of hyperphosphatemia with calcium-containing phosphate binders and treatment of hyperparathyroidism with vitamin D must be critically reviewed.
Detection of vascular and valvular calcifications can perform with echocardiography.
Volume expansion plays an important role even in the absence of visible oedema. If there is evidence of hypervolemia, therapy should supplement with a loop diuretic in conjunction with a low-sodium diet. The target blood pressure is 130/80 mmHg.

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Electrolyte Problems in Kidney Disease (verywellhealth.com)
Facts about Metabolic Acidosis and Chronic Kidney Disease | National Kidney Foundation
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Anemia Symptoms, Causes, and Treatments – American Kidney Fund (AKF)
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