Uremia is clinically defined as the active accumulation of toxic substances like nitrogenous wastes in the serum. This condition is generally brought about by the failure of the kidney to rid-off the body system with nitrogenous wastes by way of the urine. Consequently, uremia results from any medical condition that hampers the renal excretory functions.
Presentation
The following signs and symptoms are seen in patients with uremia:
- Peripheral neuropathy
- Muscular fatigue
- Seizures
- Anorexia and nausea
- Perennial cramping
- Sleep disturbances
- Coma
- Sexual dysfunction
- Bone problems
- Muscle wasting
- Pruritus
- Hiccups
- Bleeding problems
- Pallor
Workup
The following diagnostic tests and modalities are used to work up patients suffering from uremia:
- Isotope clearance: The radioisotope iothalamate is utilized to accurately measure the actual glomerular filtration rate to determine the degree of uremia in a patient.
- Complete blood count (CBC): This routine laboratory test is used to determine the level of hemoglobin and hematocrit and diagnose anemia of uremia.
- Kidney ultrasound: Renal sonograms are used to determine the presence of hydronephrosis and obstruction among patients with signs of uremia. The scan will also measure the relative size of the kidneys.
- Computed tomography (CT scan): This radiologic imaging modality can be helpful in identifying hematomas in the kidney due to trauma.
- Magnetic resonance imaging (MRI): MRI is sensitive in detecting the presence of vascular stenosis in the kidneys as a cause of uremia.
- Renal biopsy: Histopathologic studies of the kidney will reveal glomerulosclerosis in cases of long standing renal failure.
Treatment
The following treatment modalities are available for the management of uremic diseases:
- Dialysis: The use of peritoneal and hemodialysis are also implored to treat uremic states in patients. Peritoneal dialysis is usually indicated among patients with other cardiovascular conditions [7]. Hemodialysis are used for other cases but may require an arterio-venous access [8].
- Intravenous calcium gluconate: The infusion of calcium gluconate in the venous system active controls the hyperkalemic state that causes cardiac disturbances among uremic patients.
- Erythropoietic stimulating agents (ESA): These agents are arbitrarily given to promote the production of red blood cells in the bone marrows.
- Parathyroid hormone (PTH) replacement therapy: A PTH level of 150-600 pg/ml is targeted to correct the conditions of parathyroidism among ESRD patients with uremia [9].
- Oral calcium supplements: Exogenous calcium and phosphates are given to correct varying degrees of hypocalcemia and hypophosphatemia among patients with uremia.
- Diet: Studies have shown that the administration of a low protein diet among patients with uremia can lower the rate of nephron death and subsequently delay the progression to ESRD [10].
- Renal transplant: This surgical option is the definitive treatment of choice of ESRD patients with severe signs of uremia.
Prognosis
In general, uremia among ESRD patients has a very poor prognosis unless hemodialysis or renal transplantation is done promptly. However, uremia brought about by acute renal insufficiency from reversible causes like thrombocytopenic purpura, Wegener disease, and Goodpasture syndrome can have a better prognosis if diagnosed and treated early in the course of the disease. Uremic disease carries a high morbidity rating in almost all patients with concomitant diseases like diabetes mellitus and hypertension.
Etiology
Uremia usually results from chronic renal diseases caused by the following illnesses [3]:
- Polycystic kidney disease
- IgA nephropathy
- Multiple myeloma
- Uncontrolled hypertension
- Hemolytic uremic syndrome
- Goodpasture syndrome
- Thrombocytopenic purpura
- Diabetes mellitus
- Systemic lupus erythematosus
- Amyloidosis
Acute cases of renal diseases can also lead to uremia when there is a rapid rise in creatinine or urea concentrations in the blood.
Epidemiology
The actual prevalence of uremia is hard to determine because the expression of the signs and symptoms of the disease varies in some disease conditions. In normal individuals, uremic signs starts to appear at creatinine clearance level of less than 10ml/min while diabetics can have the onset of symptoms in as early as 15ml/min of creatinine clearance. Concurrently, uremia exists in patients treated as end stage renal disease (ESRD).
Almost 58% of the world’s ESRD populace resides in Brazil, Japan, Germany, USA, and Italy. The white race has higher predisposition for ESRD representing almost 60% of cases. ESRD has a slight predilection in males than their female counterparts. Mean age of onset is usually on the late adulthood stage. Patients beyond 70 years old are least likely to tolerate any delays in renal treatment for uremic signs compared to their younger counterparts.
Pathophysiology
Uremia generally develops as a complication of renal failure in most patients. There is a progressive decline in the kidney functioning during this phase where its capacity to produce adequate vital hormones, fluid and electrolyte regulation, water elimination, and acid-base homeostasis is significantly impaired. When creatinine levels go beyond 2mg/dl, the peritubular cells of the kidney fail to secrete erythropoietin that induces red blood cell formation leading to progressive anemia. By statistics, 39% of patients presenting with anemia has an associated renal dysfunction at hand [4].
The gradual accumulation of uremic toxins hampers the adhesion capacity of the thrombocytes. This impairment leads to bleeding diasthesis making ESRD patients on oral coagulopathy susceptible to pathologic bleeding in the face of uremia [5]. The breakdown in the acid-base balance by the kidney leads to the failure in the secretion of hydrogen ions and excretion of ammonium from the serum resulting to metabolic acidosis. The decreasing serum pH leads to compensatory respiration presenting as tachypnea. The accumulation of potassium secondary to tubular acidosis leads to hyperkalemia.
This is an offshoot in uremic states especially when the creatinine clearance falls below 20 mL/min. There is an imbalance in the calcium and phosphate metabolism due to the uncontrolled secretion of parathyroid hormones caused by uremia. The calcium and phosphate accumulation in the serum leads to abnormal deposition of calcium plaques in the skin, blood vessels, and other tissues in the body [6]. The uremic state will also lead to abnormal carbohydrate metabolism, sexual hormone release, and thyroid hormone secretions.
Prevention
Patients with diagnosed diabetes and hypertension should comply religiously with their maintenance medications to prevent renal complications in the future. High risk patients should avoid nephrotoxic drugs like ibuprofen and naproxen to prevent nephrotoxicity and uremia.
Summary
Uremia is a medical illness that accompanies renal failure caused by the abnormal accumulation of organic waste products normally excreted by the kidneys. Uremic symptoms clinically manifests when the glomerular filtration rate (GFR) of the kidneys fall below 60 ml per minute per 1.73 meter squared of body area [1]. Early uremic signs are usually constitutional and non-specific, thus mild uremia is oftentimes underdiagnosed. Severe uremia is corrected by renal transplant; however, the supply of kidney donors is almost always eclipsed by the demand for kidney transplant. Because of this, hemodialysis is the leading modality utilized to control and subvert this medical illness [2].
Patient Information
- Definition: Uremia is a medical condition associated with renal failure causing an abnormal accumulation of organic waste products normally excreted by the kidneys.
- Cause: Uremia can typically arise from any etiologic conditions that results in renal failure like diabetes, hypertension, multiple myeloma and SLE.
- Symptoms: Uremia will present with muscular fatigue, seizure, numbness, anorexia, and sleep disturbances.
- Diagnosis: Isotope clearance, anemia work-up, and imaging studies are diagnostic tests and modalities used in the work up of patients with uremia.
- Treatment and follow-up: Uremia can effectively be treated with dialysis and kidney transplantation.
References
- Coresh J, Byrd-Holt D, Astor BC, et al. Chronic kidney disease awareness, prevalence, and trends among U.S. adults, 1999 to 2000. J Am Soc Nephrol 2005; 16:180-188.
- USRDS 2006 annual data report: atlas of end-stage renal disease in the United States. Bethesda, MD: U.S. Renal Data System, 2006.
- Fakhouri F, Roumenina L, Provot F, et al. Pregnancy-Associated Hemolytic Uremic Syndrome Revisited in the Era of Complement Gene Mutations. J Am Soc Nephrol. Mar 4 2010.
- Almoznino-Sarafian D, Shteinshnaider M, Tzur I, et al. Anemia in diabetic patients at an internal medicine ward: Clinical correlates and prognostic significance. Eur J Intern Med. Apr 2010; 21(2):91-96.
- Boccardo P et al. (2004) Platelet dysfunction in renal failure. Semin Thromb Hemost 30: 579–589.
- Schlieper G, Aretz A, Verberckmoes SC, et al. Ultrastructural Analysis of Vascular Calcifications in Uremia.J Am Soc Nephrol. Mar 4 2010.
- Chuang YW, Shu KH, Yu TM, et al. Hypokalaemia: an independent risk factor of Enterobacteriaceae peritonitis in CAPD patients. Nephrol Dial Transplant. May 2009; 24(5):1603-8.
- Vinsonneau C, Camus C, Combes A, et al. Continuous venovenous haemodiafiltration versus intermittent haemodialysis for acute renal failure in patients with multiple-organ dysfunction syndrome: a multicentre randomised trial. Lancet2006; 368:379-385.
- KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl. Aug 2009; S1-130.
- Fouque D, Laville M. Low protein diets for chronic kidney disease in non-diabetic adults. Cochrane Database Syst Rev. Jul 8 2009; CD001892.