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Uremia is the condition of having high levels of urea in the blood. Urea is one of the primary components of urine. It can be defined as an excess in the blood of amino acid and protein metabolism end products, such as urea and creatinine, which would normally be excreted in the urine. Uremic syndrome can be defined as the terminal clinical manifestation of renal failure (also called renal failure). It is the signs, symptoms and results from laboratory tests which result from inadequate excretory, regulatory, and endocrine function of the kidneys. Both uremia and uremic syndrome have been used interchangeably to denote a very high plasma urea concentration that is the result of renal failure. The former denotation will be used for the rest of the article.
Azotemia is a similar, less severe condition with high levels of urea, where the abnormality can be measured chemically but is not yet so severe as to produce symptoms. Uremia describes the pathological and symptomatic manifestations of severe azotemia.
There is no specific time for the onset of uremia for people with progressive loss of kidney function. People with kidney function below 50% (i.e. a glomerular filtration rate GFR between 50 and 60 mL/min) and over 30 years of age may have uremia to a degree. This means an estimated 8 million people in the United States with a GFR of less than 60 mL/min have uremic symptoms. The symptoms, such as fatigue, can be very vague, making the diagnosis of impaired kidney function difficult. Treatment can be by Kidney dialysis or a kidney transplant, though some patients choose to pursue symptom control and conservative care instead.
| + Clinical features of uremia |
| diurnal somnolence, insomnia, memory and concentration disorders, asthenia, headache, confusion, fatigue, seizures, coma, encephalopathy, Hypogeusia and Hyposmia, hiccups, serositis |
| polyneuritis, restless legs, cramps, peripheral neuropathy, oxidative stress, reduced body temperature |
| anorexia, nausea, vomiting, gastroparesis, parotitis, stomatitis, superficial gastrointestinal ulcers |
| anemia, hemostasis disorders, granulocyte, lymphocyte and thrombocyte dysfunction |
| hypertension, atherosclerosis, coronary artery disease, pericarditis, Peripheral edema and pulmonary edema |
| itching, skin dryness, calciphylaxis, uremic frost (excretion of urea through the skin) |
| growth impairment, impotence, infertility, Infertility, amenorrhea |
| osteomalacia, β2-microglobulin amyloidosis, bone disease (via vitamin D deficiency, secondary hyperparathyroidism and hyperphosphatemia) |
| malnutrition, weight loss, muscular catabolism |
| uremic fetor |
| low response rate to vaccination, increased sensitivity to infectious diseases, systemic inflammation |
Glomerular filtration rate (GFR) measures the amount of plasma in millilitres being filtered through the kidneys each minute. As the GFR decreases, the prognosis worsens. Some of the effects can be reversed, albeit temporarily, with dialysis.
| + GFR and their effects |
| Normal GFR |
| Uremic symptoms may be present, reduced well-being |
| Cognitive impairment |
| Fatigue and reduced stamina |
| Insulin resistance |
| Increasing likelihood of symptoms |
| Kidney failure |
Prerenal azotemia can be caused by decreased blood flow through the kidneys (e.g. hypotension, congestive heart failure, shock, hemorrhage, dehydration) or by increased production of urea in the liver via a high protein diet or increased protein catabolism (e.g. stress, fever, major illness, corticosteroid therapy, or gastrointestinal bleeding).
Renal causes can be attributed to decreased kidney function. These include acute and chronic kidney failure, acute and chronic glomerulonephritis, tubular necrosis, and other .
Postrenal causes can be due to decreased elimination of urea. These could be due to urinary outflow obstruction such as by calculi, Neoplasm of the bladder or prostate, or a severe infection.
Urea was one of the first metabolites identified. Its removal is directly related to patient survival but its effect on the body is not yet clear. Still, it is not certain that the symptoms currently associated with uremia are actually caused by excess urea, as one study showed that uremic symptoms were relieved by initiation of dialysis, even when urea was added to the dialysate to maintain the blood urea nitrogen level at approximately 90 mg per deciliter (that is, approximately 32 mmol per liter). Urea could be the precursor of more toxic molecules, but it is more likely that damage done to the body is from a combination of different compounds which may act as or derange membrane transport. Indoxyl sulfate is one of the better characterized uremic toxins. Indoxyl sulfate has been shown to aggravate Blood vessel inflammation in atherosclerosis by modulating macrophage behavior.
| + Potential uremic toxins | |
| Induces renal dysfunction and cardiovascular dysfunction; associated with chronic kidney disease and cardiovascular disease | [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4840492/table/Tab2/ Table 2: Microbial metabolites: their synthesis, mechanisms of action, and effects on health and disease] [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4840492/figure/Fig1/ Figure 1: Molecular mechanisms of action of indole and its metabolites on host physiology and disease] |
| + Biochemistry |
| Secondary hyperparathyroidism |
| Altered thyroxine metabolism |
| Renin and hyperaldosteronism |
| Renin |
| Hypoaldosteronism |
| Decreased erythropoietin production |
| Gonadal dysfunction (increased prolactin and luteinizing hormone, decreased testosterone) |
| Increased serum gastrin and melanocyte-stimulating hormone |
One of the early symptoms of renal failure is uremic fetor. It is an ammonia odour in the mouth caused by the high concentration of urea in the saliva, which subsequently breaks down to ammonia. As the blood urea nitrogen (BUN) level increases, patients might develop uremic stomatitis. Uremic stomatitis appears as a pseudo membrane or frank ulcerations with redness and a pultaceous coat in the mouth. These lesions could be related to high BUN level (>150mg/dL), and disappear spontaneously when the BUN level is reduced with medical treatment. It is believed to be caused by loss of tissue resistance and failure to withstand traumatic influences. Besides that, the patient may develop a rare manifestation called uremic frost. It is a white plaque found on the skin or in the mouth which is caused by residual urea crystals left on the epithelial surface after perspiration and saliva evaporation, or as a result of reduced salivary flow. Xerostomia is a common oral finding. It results from a combination of direct involvement of salivary glands, chemical inflammation, dehydration and mouth breathing. It may be due to restricted fluid intake, an adverse effect of drug therapy, or low salivary rate. Salivary swelling can also be seen in some cases.
In patients with renal disease, pallor of the oral mucosa can sometimes be noticed due to anaemia caused by reduction of erythropoietin. Uraemia can lead to alteration of platelet aggregation. This situation, combined with the use of heparin and other anticoagulants in haemodialysis, causes these patients to become predisposed to ecchymosis, petechiae, and Bleeding in the oral cavity. It can also lead to mucositis and glossitis, which can bring about pain and inflammation of the tongue and oral mucosa. In addition, patients might also experience altered taste sensations (dysgeusia) and be predisposed to bacterial and candidiasis infections. Candidiasis is more frequent in renal transplant patients because of generalized immunosuppression.
In children with renal disease, enamel hypoplasia of the primary and permanent dentition has been observed. The abnormalities of dental development correlate with the age at which metabolic disturbances occur. For example, enamel hypoplasia in the form of white or brown discoloration of primary teeth is commonly seen in young children with early-onset renal disease. Poor oral hygiene, a carbohydrate-rich diet, disease-related debilitation, hypoplastic enamel, low salivary flow rate and long-term medication contribute to increased risk of Tooth decay formation. However, the patients usually have low cavity activity, particularly in children. This is due to the presence of highly buffered and alkaline saliva caused by the high concentration of urea nitrogen and phosphate in saliva. The salivary pH will usually be above the critical pH level for demineralization of the enamel to occur, and this helps to prevent the formation of cavities. Besides that, pulpal narrowing and calcifications are a frequent finding in patients with renal disease. For patients who are on dialysis, the nausea and vomiting resulting from dialysis treatment may lead to severe Acid erosion.
Dental examination for such patients consists of a non-invasive complete assessment of dental, periodontal, and mucosal tissues, with radiographs to aid with the diagnostic process. All potential foci of infection should be intercepted; these include periodontal and endodontic lesions, residual roots, partially erupted and malpositioned third molars, peri-implantitis, and mucosal lesions. When periodontitis is suspected, a periodontal chart should be recorded. Orthodontic appliances can be maintained if they do not interfere with oral hygiene.
Uremia is commonly seen in patients who undergo dialysis due to renal insufficiency. For hemodialysis patients, it is important to determine the treatment schedule. Dental treatment should be started on the day after hemodialysis due to several reasons: there is no accumulation of uremic toxins in the blood, and circulating heparin is absent. Treatment should not commence on the same day as hemodialysis as patients usually feel unwell and their blood is heparinized, which might cause excessive bleeding. For patients undergoing peritoneal dialysis, there are no contraindications to dental treatment except in cases of acute peritoneal infections, where elective procedure should be deferred.
Special care should be taken when positioning the patient, avoiding compression of the arm with the vascular access for hemodialysis. Any injections or blood pressure measurement should not be performed on an arm with an arteriovenous (AV) fistula. If the AV site is located on a leg, the patient should avoid sitting for lengthy periods, as venous drainage may be obstructed. During long dental procedures, the dentist should allow patients with AV sites on their legs to take a brief walk or stand for a while every hour.
Hemostatic aids should be instituted in cases of excessive bleeding, which is commonly seen in uremia and renal failure. To manage postoperative bleeding, primary closure techniques and local hemostatic agents should be used routinely. To reduce bleeding during and after a procedure, tranexamic acid, both as a rinse or administered orally, can be used.
Patients undergoing dialysis are exposed to numerous transfusions and renal failure-related immunosuppression; thus, they are at greater risks of infection by human immunodeficiency virus (HIV) and hepatitis types B and C. It is important to adopt infection control measures to avoid cross-contamination in the dental clinic and prevent risk of exposure to dental personnel.
A majority of medications are eliminated from the body at least partially by the kidney. Due to renal failure, the plasma half-lives of drugs normally excreted in urine will be prolonged, leading to increased toxicity. Many drugs which are normally safely administered cannot be given to patients with reduced renal function. Besides, some drugs can be given, but the dosage must be reduced. However, in patients undergoing dialysis, reduced plasma half-lives of drugs will be observed. Antibiotics of the aminoglycoside and tetracycline families need to be avoided due to their nephrotoxicities. The antibiotics of choice are penicillins, clindamycin, and cephalosporins, which can be administered at normal doses even if the therapeutic range will be extended. For analgesics, paracetamol is the option of choice for cases of episodic pain. Aspirin is characterized by an anti-platelet activity and thus its use should be avoided in uremic patients. The challenge in pharmacotherapy for patients with renal disease is to maintain a medication's therapeutic level within a narrow range in order to avoid subtherapeutic dosing and toxicity.
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