A biochemical abnormality referring to an elevation of BLOOD UREA NITROGEN and CREATININE. Azotemia can be produced by KIDNEY DISEASES or other extrarenal disorders. When azotemia becomes associated with a constellation of clinical signs, it is termed UREMIA.
A clinical syndrome associated with the retention of renal waste products or uremic toxins in the blood. It is usually the result of RENAL INSUFFICIENCY. Most uremic toxins are end products of protein or nitrogen CATABOLISM, such as UREA or CREATININE. Severe uremia can lead to multiple organ dysfunctions with a constellation of symptoms.
The urea concentration of the blood stated in terms of nitrogen content. Serum (plasma) urea nitrogen is approximately 12% higher than blood urea nitrogen concentration because of the greater protein content of red blood cells. Increases in blood or serum urea nitrogen are referred to as azotemia and may have prerenal, renal, or postrenal causes. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.
A congenital or acquired condition of insufficient production of ALDOSTERONE by the ADRENAL CORTEX leading to diminished aldosterone-mediated synthesis of Na(+)-K(+)-EXCHANGING ATPASE in renal tubular cells. Clinical symptoms include HYPERKALEMIA, sodium-wasting, HYPOTENSION, and sometimes metabolic ACIDOSIS.
Acute kidney failure resulting from destruction of EPITHELIAL CELLS of the KIDNEY TUBULES. It is commonly attributed to exposure to toxic agents or renal ISCHEMIA following severe TRAUMA.
Creatinine is a waste product that's generated from muscle metabolism, typically filtered through the kidneys and released in urine, with increased levels in blood indicating impaired kidney function.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Excision of kidney.
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.
Pathological processes of the KIDNEY or its component tissues.
A significant drop in BLOOD PRESSURE after assuming a standing position. Orthostatic hypotension is a finding, and defined as a 20-mm Hg decrease in systolic pressure or a 10-mm Hg decrease in diastolic pressure 3 minutes after the person has risen from supine to standing. Symptoms generally include DIZZINESS, blurred vision, and SYNCOPE.
Absence of urine formation. It is usually associated with complete bilateral ureteral (URETER) obstruction, complete lower urinary tract obstruction, or unilateral ureteral obstruction when a solitary kidney is present.
Inorganic compounds that contain nitrogen as an integral part of the molecule.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
Decreased URINE output that is below the normal range. Oliguria can be defined as urine output of less than or equal to 0.5 or 1 ml/kg/hr depending on the age.

A scoring system to predict renal outcome in IgA nephropathy: from a nationwide prospective study. (1/22)

BACKGROUND: Immunoglobulin A (IgA) nephropathy is the most common form of glomerulonephritis in the world, and a substantial number of patients develop end-stage renal disease (ESRD). Although there are several prognostic indicators, it remains difficult to predict the renal outcome in individual patients. METHODS: A prospective cohort study was conducted in 97 clinical units in Japan from 1995 to 2002. We analysed the data from 2269 patients using proportional hazards models in order to determine the predictors of ESRD in IgA nephropathy and to develop a scoring system to estimate ESRD risk. RESULTS: During the follow-up (median, 77 months), 207 patients developed ESRD. Systolic hypertension, proteinuria, hypoproteinaemia, azotaemia and a high histological grade at initial renal biopsy were independently associated with the risk of ESRD. Mild haematuria predisposed patients to ESRD more than severe haematuria. A scoring system was developed to estimate the 7-year ESRD risk from eight clinical and pathological variables. Actually, this prognostic score accurately classified patients by risk: patients with estimates of 0.0-0.9, 1.0-4.9, 5.0-19.9, 20.0-49.9, and 50.0-100.0% had a 0.2, 2.4, 12.2, 40.2 and 80.8% of ESRD incidence over 7 years, respectively. The corresponding area under the receiver operating characteristic curve was 0.939 [95% confidence interval (CI), 0.921-0.958]. This score was verified in repetitions of the derivation-validation technique. CONCLUSIONS: Although the quality of some data collected by the mail survey is limited and the influence of therapy could not be considered, this scoring system will serve as a useful prognostic tool for IgA nephropathy in clinical practice.  (+info)

Clinical research on navel application of Shehuang Paste combined with Chinese herbal colon dialysis in treatment of refractory cirrhotic ascites complicated with azotemia. (2/22)

AIM: To explore the efficacy and mechanism of a novel therapeutic method of traditional Chinese medicine in patients with refractory cirrhotic ascites complicated with azotemia. METHODS: Seventy-five cases of refractory cirrhotic ascites complicated with azotemia were randomly divided into 3 groups: comprehensive treatment (n = 29), simple treatment (n = 24), and control (n = 22). The basic treatment methods were the same in all groups, including liver protecting medicines, diuretics and supportive drugs. The control group underwent only the basic treatment. Shehuang Paste (SHP) was applied to the navels of the two treatment groups once a day for 30 d. Colon dialysis with Chinese herbs was administered to the comprehensive treatment group once every two days. Before and after treatment, we measured abdominal circumference, BUN, Cr, serum Na+, urine Na+/K+, liver function, endotoxin content, NO, and ET-1. Color Doppler ultrasonography was conducted to measure the portal vein blood flow. RESULTS: The total effective rate for ascites was 72.4% in the comprehensive treatment group, 45.8% in the simple treatment, contrasting with 18.2% in the controls. Between the two treatment groups and the controls, there were significant differences in the effective rates (P < 0.01, and P < 0.05). There was also a significant difference (P < 0.05) between the two treatment groups. Measurements of Cr and BUN showed higher values for the treatment groups, with the comprehensive better than the simple group (P < 0.05). Sera Na, urine Na/K were different, P < 0.01 between pre- and post-treatment in the comprehensive group, and P < 0.05 in the simple group. The treatment groups' endotoxin content was also significantly reduced (P < 0.01, and P < 0.05), with the comprehensive group better than the simple group (P < 0.05). Portal vein blood flow and NO content significantly reduced (P < 0.05), as did ET-1 content (P < 0.01). There were no significant changes in the control group (P > 0.05). The comprehensive treatment group's pre- and post-treatment portal vein and splenic vein blood flows showed a positive correlation to NO, ET-1 and endotoxin contents. CONCLUSION: When treating refractory cirrhotic ascites complicated with azotemia, Shehuang Paste combined with Chinese herbal dialysis is better than Shehuang Paste alone for ascites resolution, azotemia, and endotoxin elimination. However, both methods on their own were also effective for reducing portal and splenic vein blood flow, and lowering the contents of NO, ET-1 in the two treatment groups.  (+info)

A preliminary report of brain edema in patients with uremia at first hemodialysis: evaluation by diffusion-weighted MR imaging. (3/22)

BACKGROUND AND PURPOSE: The dynamics of brain-water content associated with hemodialysis in patients with severe azotemia remains obscure. To investigate whether either interstitial or cytotoxic edema is responsible for dialysis disequilibrium syndrome (DDS), we used diffusion-weighted MR imaging (DWI) to measure the apparent diffusion coefficient (ADC), which is sensitive for detecting tissue water dynamics. METHODS: Eight consecutive patients with end stage renal disease (ESRD) and blood urea nitrogen level of more than 100 mg/dL (160.9 +/- 53.1 mg/dL) were recruited. Conventional MR images, DWI, and clinical manifestations were obtained before and after the 1st hemodialysis. The ADC values were determined for regions of normal-appearing gray and white matter and for regions of hyperintensity of white matter on T2-weighted MR imaging. RESULTS: Foci of bright areas of white matter were found in all patients on T2-weighted images. The ADC values of the patients with ESRD, in white matter and gray matter before and after hemodialysis, were greater than those of the healthy controls (P < .005). Regarding the impact of hemodialysis, the ADC of frontal lobe white matter increased significantly after hemodialysis (1.09 +/- 0.11 versus 1.03 +/- 0.11, P = .036). We did not find the specific area of brain edema reported in posterior leukoencephalopathy and the osmotic demyelination syndrome. CONCLUSIONS: These results suggest that severe azotemia in end stage renal disease leads to interstitial brain edema reflected as increased ADC, and the further increased ADC reflects that edema associated with 1st hemodialysis is interstitial rather than cytotoxic in nature.  (+info)

Carbon dioxide digital subtraction angiography-assisted endovascular aortic aneurysm repair in the azotemic patient. (4/22)

OBJECTIVE: This report analyzes the safety and efficacy of carbon dioxide digital subtraction angiography (CO(2)-DSA) for EVAR in a group of patients with renal insufficiency compared with a concurrent group of patients with normal renal function undergoing EVAR with iodinated contrast angiography (ICA). METHODS: Between 2003 and 2005, 100 consecutive patients who underwent EVAR using ICA, CO(2)-DSA, or both were retrospectively reviewed, and preoperative, intraoperative, postoperative, and follow-up variables were collected. Patients were divided into two groups depending on renal function and contrast used. Group I comprised patients with normal renal function in whom ICA was used exclusively, and group II patients had a serum creatinine >or=1.5 mg/dL, and CO(2)-DSA was used preferentially and supplemented with ICA, when necessary. The two groups were compared for the outcomes of successful graft placement, renal function, endoleak type, and frequency, and the need for graft revision. Comparisons were made using chi(2) analysis, Student t test, and the Fisher exact test. RESULTS: A total of 84 EVARs were performed in group I and 16 in group II. Patient demographics and risk factors were similar between groups with the exception of serum creatinine, which was significantly increased in group II (1.8 mg/dL vs 1.0 mg/dL P < .0005). All 100 endografts were successfully implanted. Patients in group II had longer fluoroscopy times, longer operative times, and increased radiation exposure, and 13 of 16 patients required supplemental ICA. Mean iodinated contrast use was 27 mL for group II vs 148 mL in group I (P < .0005). Mean postoperative serum creatinine was unchanged from baseline, and 30-day morbidity was similar for both groups. No patient required dialysis. No patients died. Perioperatively, and at 1 and 6 months, the endoleak type and incidence and need for endograft revision was no different between groups. CONCLUSIONS: CO(2)-DSA is safe, can be used to guide EVAR, and provides outcomes similar to ICA-guided EVAR. CO2-DSA protects renal function in the azotemic patient by lessening the need for iodinated contrast and associated nephrotoxicity, but with the tradeoff of longer fluoroscopy and operating room times and increased radiation exposure.  (+info)

Timing of initiation of dialysis in critically ill patients with acute kidney injury. (5/22)

Among critically ill patients, acute kidney injury (AKI) is a relatively common complication that is associated with an increased risk for death and other complications. To date, no treatment has been developed to prevent or attenuate established AKI. Dialysis often is required, but the optimal timing of initiation of dialysis is unknown. Data from the Program to Improve Care in Acute Renal Disease (PICARD), a multicenter observational study of AKI, were analyzed. Among 243 patients who did not have chronic kidney disease and who required dialysis for severe AKI, we examined the risk for death within 60 d from the diagnosis of AKI by the blood urea nitrogen (BUN) concentration at the start of dialysis (BUN < or = 76 mg/dl in the low degree of azotemia group [n = 122] versus BUN > 76 mg/dl in the high degree of azotemia group [n = 121]). Standard Kaplan-Meier product limit estimates, proportional hazards (Cox) regression methods, and a propensity score approach were used to account for selection effects. Crude survival rates were slightly lower for patients who started dialysis at higher BUN concentrations, despite a lesser burden of organ system failure. Adjusted for age, hepatic failure, sepsis, thrombocytopenia, and serum creatinine and stratified by site and initial dialysis modality, the relative risk for death that was associated with initiation of dialysis at a higher BUN was 1.85 (95% confidence interval 1.16 to 2.96). Further adjustment for the propensity score did not materially alter the association (relative risk 1.97; 95% confidence interval 1.21 to 3.20). Among critically ill patients with AKI, initiation of dialysis at higher BUN concentrations was associated with an increased risk for death. Although the results could reflect residual confounding by severity of illness, they provide a rationale for prospective testing of alternative dialysis initiation strategies in critically ill patients with severe AKI.  (+info)

Sensitivity and specificity of a single emergency department measurement of urinary neutrophil gelatinase-associated lipocalin for diagnosing acute kidney injury. (6/22)

BACKGROUND: A single serum creatinine measurement cannot distinguish acute kidney injury from chronic kidney disease or prerenal azotemia. OBJECTIVE: To test the sensitivity and specificity of a single measurement of urinary neutrophil gelatinase-associated lipocalin (NGAL) and other urinary proteins to detect acute kidney injury in a spectrum of patients. DESIGN: Prospective cohort study. SETTING: Emergency department of Columbia University Medical Center, New York, New York. PARTICIPANTS: 635 patients admitted to the hospital with acute kidney injury, prerenal azotemia, chronic kidney disease, or normal kidney function. MEASUREMENTS: Diagnosis of acute kidney injury was based on the RIFLE (risk, injury, failure, loss, and end-stage) criteria and assigned by researchers who were blinded to experimental measurements. Urinary NGAL was measured by immunoblot, N-acetyl-beta-d-glucosaminidase (NAG) by enzyme measurement, alpha1-microglobulin and alpha(1)-acid glycoprotein by immunonephelometry, and serum creatinine by Jaffe kinetic reaction. Experimental measurements were not available to treating physicians. RESULTS: Patients with acute kidney injury had a significantly elevated mean urinary NGAL level compared with the other kidney function groups (416 microg/g creatinine [SD, 387]; P = 0.001). At a cutoff value of 130 microg/g creatinine, sensitivity and specificity of NGAL for detecting acute injury were 0.900 (95% CI, 0.73 to 0.98) and 0.995 (CI, 0.990 to 1.00), respectively, and positive and negative likelihood ratios were 181.5 (CI, 58.33 to 564.71) and 0.10 (CI, 0.03 to 0.29); these values were superior to those for NAG, alpha1-microglobulin, alpha1-acid glycoprotein, fractional excretion of sodium, and serum creatinine. In multiple logistic regression, urinary NGAL level was highly predictive of clinical outcomes, including nephrology consultation, dialysis, and admission to the intensive care unit (odds ratio, 24.71 [CI, 7.69 to 79.42]). LIMITATIONS: All patients came from a single center. Few kidney biopsies were performed. CONCLUSION: A single measurement of urinary NGAL helps to distinguish acute injury from normal function, prerenal azotemia, and chronic kidney disease and predicts poor inpatient outcomes.  (+info)

Impact of renal failure on survival of African patients with cirrhosis. (7/22)

To assess the effect of renal failure on the survival of black African patients with cirrhosis, we studied 132 (82 males, 50 females) cirrhotic black African patients with mean age of 47.5+/-14.4 years and mean follow-up period of 373+/-194 days. The edema and ascitis were the main reasons for admission to hospital. Renal failure was present in 30 (22.7%) patients, and it was positively correlated to the severity of the stage of the liver disease, and associated with severe hyponatremia. Survival at 1 year was 60.1% and 37.6% in the absence or presence of renal failure, respectively (p<0.001)). The stage of the liver disease was significantly inversely correlated with survival, which was further diminished in the presence of renal failure:23.7% versus 12.5% for Child-Pugh-Turcote (CPT) A-B in the absence or presence of renal failure, respectively (p=0.67), 30.2% versus 81.8% for CPT C in the absence or the presence of renal failure respectively (p<0.001). Hyponatremia has also appeared detrimental to survival, since mortality was 38.4% versus 81.8% in the absence or the presence of hyponatremia respectively (p<0.001). By multivariate analysis, renal failure, CPT stage C, and hyponatremia independently significantly correlated to mortality in patients with cirrhosis. We conclude that renal failure is frequently associated with decompensated cirrhosis. The presence of renal failure in this setting often results in high mortality. Renal failure that occurs in the setting of a severe liver disease and hyponatremia may be part of hepatorenal syndrome.  (+info)

Uremia induces proximal tubular cytoresistance and heme oxygenase-1 expression in the absence of acute kidney injury. (8/22)

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Azotemia is a medical term that refers to an elevated level of urea and other nitrogenous waste products in the blood. This condition is typically caused by impaired kidney function, which can lead to the accumulation of these substances in the body.

Normally, the kidneys filter waste products from the blood and excrete them in the urine. However, when the kidneys are not functioning properly, they may be unable to remove these waste products efficiently, leading to their buildup in the bloodstream. This can cause a range of symptoms, including nausea, vomiting, fatigue, and confusion.

Azotemia is often classified based on the level of urea in the blood, with mild azotemia defined as a blood urea nitrogen (BUN) level between 20 and 39 mg/dL, moderate azotemia defined as a BUN level between 40 and 89 mg/dL, and severe azotemia defined as a BUN level of 90 mg/dL or higher.

Treatment for azotemia typically involves addressing the underlying cause of the condition, which may involve medications to control high blood pressure or diabetes, dietary changes, or dialysis in severe cases.

Uremia is not a disease itself, but rather it's a condition that results from the buildup of waste products in the blood due to kidney failure. The term "uremia" comes from the word "urea," which is one of the waste products that accumulate when the kidneys are not functioning properly.

In uremia, the kidneys are unable to effectively filter waste and excess fluids from the blood, leading to a variety of symptoms such as nausea, vomiting, fatigue, itching, mental confusion, and ultimately, if left untreated, can lead to coma and death. It is a serious condition that requires immediate medical attention, often involving dialysis or a kidney transplant to manage the underlying kidney dysfunction.

Blood Urea Nitrogen (BUN) is a laboratory value that measures the amount of urea nitrogen in the blood. Urea nitrogen is a waste product that is formed when proteins are broken down in the liver. The kidneys filter urea nitrogen from the blood and excrete it as urine.

A high BUN level may indicate impaired kidney function, as the kidneys are not effectively removing urea nitrogen from the blood. However, BUN levels can also be affected by other factors such as dehydration, heart failure, or gastrointestinal bleeding. Therefore, BUN should be interpreted in conjunction with other laboratory values and clinical findings.

The normal range for BUN is typically between 7-20 mg/dL (milligrams per deciliter) or 2.5-7.1 mmol/L (millimoles per liter), but the reference range may vary depending on the laboratory.

Acute kidney injury (AKI), also known as acute renal failure, is a rapid loss of kidney function that occurs over a few hours or days. It is defined as an increase in the serum creatinine level by 0.3 mg/dL within 48 hours or an increase in the creatinine level to more than 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days, or a urine volume of less than 0.5 mL/kg per hour for six hours.

AKI can be caused by a variety of conditions, including decreased blood flow to the kidneys, obstruction of the urinary tract, exposure to toxic substances, and certain medications. Symptoms of AKI may include decreased urine output, fluid retention, electrolyte imbalances, and metabolic acidosis. Treatment typically involves addressing the underlying cause of the injury and providing supportive care, such as dialysis, to help maintain kidney function until the injury resolves.

Hypoaldosteronism is a medical condition characterized by decreased levels or impaired function of the hormone aldosterone, which is produced by the adrenal gland. Aldosterone plays a crucial role in regulating electrolyte and fluid balance in the body by increasing the reabsorption of sodium and excretion of potassium in the kidneys.

Hypoaldosteronism can lead to low blood pressure, muscle weakness, and an imbalance of electrolytes, particularly low serum sodium levels and high serum potassium levels. This condition can be caused by various factors, including damage to the adrenal gland, impaired production or function of aldosterone, or decreased responsiveness of the kidneys to aldosterone.

Hypoaldosteronism can be primary or secondary. Primary hypoaldosteronism is caused by a problem with the adrenal glands themselves, such as damage to the gland or a genetic disorder that affects aldosterone production. Secondary hypoaldosteronism is caused by a problem outside of the adrenal glands, such as decreased production of renin (an enzyme produced by the kidneys) or certain medications that interfere with aldosterone production or function.

Treatment for hypoaldosteronism depends on the underlying cause and may include medication to replace missing aldosterone or correct electrolyte imbalances, as well as addressing any underlying conditions contributing to the development of the condition.

Acute Kidney Tubular Necrosis (ATN) is a medical condition characterized by the death of tubular epithelial cells that make up the renal tubules of the kidneys. This damage can occur as a result of various insults, including ischemia (lack of blood flow), toxins, or medications.

In ATN, the necrosis of the tubular cells leads to a decrease in the kidney's ability to concentrate urine, regulate electrolytes and remove waste products from the body. This can result in symptoms such as decreased urine output, fluid and electrolyte imbalances, and the accumulation of waste products in the blood (azotemia).

Acute Kidney Tubular Necrosis is usually diagnosed based on clinical findings, laboratory tests, and imaging studies. Treatment typically involves supportive care, such as administering intravenous fluids to maintain hydration and electrolyte balance, managing any underlying conditions that may have contributed to the development of ATN, and providing dialysis if necessary to support kidney function until the tubular cells can recover.

Creatinine is a waste product that's produced by your muscles and removed from your body by your kidneys. Creatinine is a breakdown product of creatine, a compound found in meat and fish, as well as in the muscles of vertebrates, including humans.

In healthy individuals, the kidneys filter out most of the creatinine and eliminate it through urine. However, when the kidneys are not functioning properly, creatinine levels in the blood can rise. Therefore, measuring the amount of creatinine in the blood or urine is a common way to test how well the kidneys are working. High creatinine levels in the blood may indicate kidney damage or kidney disease.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

Nephrectomy is a surgical procedure in which all or part of a kidney is removed. It may be performed due to various reasons such as severe kidney damage, kidney cancer, or living donor transplantation. The type of nephrectomy depends on the reason for the surgery - a simple nephrectomy involves removing only the affected portion of the kidney, while a radical nephrectomy includes removal of the whole kidney along with its surrounding tissues like the adrenal gland and lymph nodes.

Proteinuria is a medical term that refers to the presence of excess proteins, particularly albumin, in the urine. Under normal circumstances, only small amounts of proteins should be found in the urine because the majority of proteins are too large to pass through the glomeruli, which are the filtering units of the kidneys.

However, when the glomeruli become damaged or diseased, they may allow larger molecules such as proteins to leak into the urine. Persistent proteinuria is often a sign of kidney disease and can indicate damage to the glomeruli. It is usually detected through a routine urinalysis and may be confirmed with further testing.

The severity of proteinuria can vary, and it can be a symptom of various underlying conditions such as diabetes, hypertension, glomerulonephritis, and other kidney diseases. Treatment for proteinuria depends on the underlying cause and may include medications to control blood pressure, manage diabetes, or reduce protein loss in the urine.

Chronic kidney failure, also known as chronic kidney disease (CKD) stage 5 or end-stage renal disease (ESRD), is a permanent loss of kidney function that occurs gradually over a period of months to years. It is defined as a glomerular filtration rate (GFR) of less than 15 ml/min, which means the kidneys are filtering waste and excess fluids at less than 15% of their normal capacity.

CKD can be caused by various underlying conditions such as diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and recurrent kidney infections. Over time, the damage to the kidneys can lead to a buildup of waste products and fluids in the body, which can cause a range of symptoms including fatigue, weakness, shortness of breath, nausea, vomiting, and confusion.

Treatment for chronic kidney failure typically involves managing the underlying condition, making lifestyle changes such as following a healthy diet, and receiving supportive care such as dialysis or a kidney transplant to replace lost kidney function.

Kidney disease, also known as nephropathy or renal disease, refers to any functional or structural damage to the kidneys that impairs their ability to filter blood, regulate electrolytes, produce hormones, and maintain fluid balance. This damage can result from a wide range of causes, including diabetes, hypertension, glomerulonephritis, polycystic kidney disease, lupus, infections, drugs, toxins, and congenital or inherited disorders.

Depending on the severity and progression of the kidney damage, kidney diseases can be classified into two main categories: acute kidney injury (AKI) and chronic kidney disease (CKD). AKI is a sudden and often reversible loss of kidney function that occurs over hours to days, while CKD is a progressive and irreversible decline in kidney function that develops over months or years.

Symptoms of kidney diseases may include edema, proteinuria, hematuria, hypertension, electrolyte imbalances, metabolic acidosis, anemia, and decreased urine output. Treatment options depend on the underlying cause and severity of the disease and may include medications, dietary modifications, dialysis, or kidney transplantation.

Orthostatic hypotension is a type of low blood pressure that occurs when you stand up from a sitting or lying position. The drop in blood pressure causes a brief period of lightheadedness or dizziness, and can even cause fainting in some cases. This condition is also known as postural hypotension.

Orthostatic hypotension is caused by a rapid decrease in blood pressure when you stand up, which reduces the amount of blood that reaches your brain. Normally, when you stand up, your body compensates for this by increasing your heart rate and constricting blood vessels to maintain blood pressure. However, if these mechanisms fail or are impaired, orthostatic hypotension can occur.

Orthostatic hypotension is more common in older adults, but it can also affect younger people who have certain medical conditions or take certain medications. Some of the risk factors for orthostatic hypotension include dehydration, prolonged bed rest, pregnancy, diabetes, heart disease, Parkinson's disease, and certain neurological disorders.

If you experience symptoms of orthostatic hypotension, it is important to seek medical attention. Your healthcare provider can perform tests to determine the underlying cause of your symptoms and recommend appropriate treatment options. Treatment may include lifestyle changes, such as increasing fluid intake, avoiding alcohol and caffeine, and gradually changing positions from lying down or sitting to standing up. In some cases, medication may be necessary to manage orthostatic hypotension.

Anuria is a medical condition characterized by the absence or near-absence of urine output, typically defined as less than 100 milliliters in 24 hours. This occurs when the kidneys are unable to produce urine due to a complete or nearly complete failure of both kidneys' function. Anuria can be caused by various underlying medical conditions such as severe dehydration, kidney damage, obstruction in the urinary tract, or certain medications that affect kidney function. It is considered a serious medical emergency and requires immediate evaluation and treatment to prevent further complications, including potential permanent kidney damage or even death.

Nitrogen compounds are chemical substances that contain nitrogen, which is a non-metal in group 15 of the periodic table. Nitrogen forms compounds with many other elements due to its ability to form multiple bonds, including covalent bonds with hydrogen, oxygen, carbon, sulfur, and halogens.

Nitrogen can exist in several oxidation states, ranging from -3 to +5, which leads to a wide variety of nitrogen compounds with different properties and uses. Some common examples of nitrogen compounds include:

* Ammonia (NH3), a colorless gas with a pungent odor, used in fertilizers, cleaning products, and refrigeration systems.
* Nitric acid (HNO3), a strong mineral acid used in the production of explosives, dyes, and fertilizers.
* Ammonium nitrate (NH4NO3), a white crystalline solid used as a fertilizer and explosive ingredient.
* Hydrazine (N2H4), a colorless liquid with a strong odor, used as a rocket fuel and reducing agent.
* Nitrous oxide (N2O), a colorless gas used as an anesthetic and laughing gas in dental procedures.

Nitrogen compounds have many important applications in various industries, such as agriculture, pharmaceuticals, chemicals, and energy production. However, some nitrogen compounds can also be harmful or toxic to humans and the environment if not handled properly.

An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.

Oliguria is a medical term that refers to a condition where the urine output is significantly reduced, typically defined as less than 400 milliliters (or about 13 ounces) in 24 hours for an adult. This condition can be a sign of underlying kidney dysfunction or other medical conditions that affect urine production, such as dehydration, shock, or obstruction of the urinary tract. It is important to note that oliguria can be a serious symptom and requires prompt medical attention to determine the cause and initiate appropriate treatment.

Azotemia has three classifications, depending on its causative origin: prerenal azotemia, renal azotemia, and postrenal ... Stasis of urine in post-renal azotemia has the same effect.[citation needed] Prompt treatment of some causes of azotemia can ... Like in prerenal azotemia, there is no inherent renal disease. The increased resistance to urine flow can cause back up into ... Prerenal azotemia is caused by a decrease in blood flow (hypoperfusion) to the kidneys. However, there is no inherent kidney ...
Prerenal azotemia is an abnormally high level of nitrogen waste products in the blood. ... Prerenal azotemia is an abnormally high level of nitrogen waste products in the blood. ... Prerenal azotemia may have no symptoms. Or, symptoms of the causes of prerenal azotemia may be present. ... Prerenal azotemia can be reversed if the cause can be found and corrected within 24 hours. If the cause is not fixed quickly, ...
Azotemia is an elevation of blood urea nitrogen (BUN) and serum creatinine levels. The reference range for BUN is 8-20 mg/dL, ... Intrarenal azotemia. Intrarenal azotemia, also known as acute kidney injury (AKI), renal-renal azotemia, and (in the past) ... Prerenal azotemia. Prerenal azotemia refers to elevations in BUN and creatinine levels resulting from problems in the systemic ... Postrenal azotemia. Postrenal azotemia refers to elevations in BUN and creatinine levels resulting from obstruction in the ...
... -- Meet all voters on Definitions.net ... List of voters for the definition of azotaemia. This page is about the voters of the definition of azotaemia.. ... Share your thoughts on this azotaemia definition with the community:. https://www.definitions.net/definition-voters/wikipedia/ ...
Calcium and Phosphate Homeostasis in Hyperthyroid Cats - Associations with Development of Azotaemia and Survival Time. ... were performed to identify if parathyroid hormone and fibroblast growth factor-23 were predictors of development of azotaemia ... plasma parathyroid hormone and fibroblast growth factor-23 concentrations were not predictors of the development of azotaemia ...
Azotemia is an elevation of blood urea nitrogen (BUN) and serum creatinine levels. The reference range for BUN is 8-20 mg/dL, ... encoded search term (Azotemia) and Azotemia What to Read Next on Medscape ... Azotemia Differential Diagnoses. Updated: Feb 12, 2016 * Author: Moro O Salifu, MD, MPH, FACP; Chief Editor: Vecihi Batuman, MD ... Diagnostic indices in azotemia. Although such indices are helpful, it is not necessary to perform all these tests on every ...
Noun azotemia has 1 sense. *azotemia(n = noun.state) azotaemia, uraemia, uremia - accumulation in the blood of nitrogenous ... Table of Contents -- azotemia. POS HYPHEN WORDNET DICTIONARY CIDE DICTIONARY Link, Gadget and Share ... azotemia, n. the accumulation of an abnormally large amount of nitrogen-containing waste products, such as urea, in the blood; ... a href="http://kamus.sabda.org/dictionary/azotemia",azotemia,/a,. Gadget Indonesia English. ...
... a condition called azotemia can develop, and the effects may be life-threatening. ... Postrenal Azotemia. Postrenal azotemia relates to the process after kidney filtration, describing a problem in the ureters or ... Intrinsic Azotemia. Intrinsic azotemia affects kidney structure and prevents them from working properly. The deformity could be ... Treating postrenal azotemia includes removing the obstruction in the vessel and initiating rehydration. Intrinsic azotemia is a ...
Learn and reinforce your understanding of Postrenal azotemia. ... Postrenal azotemia can lead to kidney failure if left untreated ... Postrenal azotemia Videos, Flashcards, High Yield Notes, & Practice Questions. ... azotemia) due to obstruction of the urinary tract. Postrenal azotemia can be caused by congenital abnormalities such as ... Postrenal azotemia is a condition characterized by an excessive level of nitrogen-containing waste products in the bloodstream ...
Azotemia Azotemia, presumably prerenal azotemia, may be precipitated during the administration of metolazone tablets, USP. If ... azotemia and oliguria worsen during treatment of patients with severe renal disease, metolazone tablets, USP, should be ...
Azotemia Azotemia, presumably prerenal azotemia, may be precipitated during the administration of metolazone. If azotemia and ...
How to use azotemia in a sentence?. azotemia in a sentence. The BUN : Cr in prerenal azotemia is greater than 20. The BUN : Cr ... What is the prognosis of azotemia?. Azotemia Prognosis. Many individuals affected with prerenal and postrenal forms of Azotemia ... What does azotemia mean?. The definition of azotemia is having an unusually high amount of nitrogen waste product in your ... The BUN : Cr in postrenal azotemia is initially , 15. Stasis of urine in post-renal azotemia has the same effect. Uremia is the ...
Azotemia. Prerenal azotemia is an abnormally high level of nitrogen waste products in the blood. ... Limiting protein in the diet can help control the buildup of waste products in the blood ( azotemia ) that can lead to symptoms ...
Azotemia. Tyagi A, Aeddula NR. Tyagi A, et al. 2023 May 14. In: StatPearls [Internet]. Treasure Island (FL): StatPearls ...
Prolonged hypernatremia associated with azotemia and hyponatriuria. The American journal of medicine, 86(4), 494-496. https:// ...
mild, transient proteinuria and azotemia (5) Chimpanzee iv Mild, transient proteinuria and azotemia (5) ...
A suspected case of hypoxia-induced pre-renal azotemia in an old part-Arab stallion: case report and review of the literature ... AGINA, O. A., & ANI, E. C. (2020). A suspected case of hypoxia-induced pre-renal azotemia in an old part-Arab stallion: case ... hematology; hypoxia; serum biochemistry; old stallion; part-Arab; pre-renal azotemia Abstract. The kidneys maintain homeostasis ... A study to evaluate the role of bun/creatinine ratio as a discriminator factor in azotemia. International Journal of ...
The purpose of this study was to evaluate if prevention of this transient hypothyroidism would blunt the progression of azote- mia ... Use of L-Thyroxine Supplementation after Radioiodine Therapy Helps Blunt the Worsening of Azotemia in Hyperthyroid Cats with ... 2010;24:1086). In hyperthyroid cats with concurrent azotemia, the transient hypothyroidism that fol- lows radioiodine therapy ... Iatrogenic hypothyroidism has been shown to contribute to worsening of azotemia and shortened life expectancy in cats with pre- ...
All patients were divided into 26 pts (mean: 60.0 ± 15.15 years) with prerenal azotemia (group-1) and 14 pts (mean: 56.29 ± ... Fractional excretion of sodium (FENa) is used to differentiate renal from prerenal azotemia. However, many drugs and medical ... For differentiating renal from prerenal azotemia; compared to FENa, FEurea showed better sensitivity (78.1 % vs. 71.4%) and ... Fractional excretion of sodium and fractional excretion of urea in differentiating prerenal from renal azotemia complicating ...
Prerenal azotemia may also be present.. Laboratory Features of Polycythemias. Relative. Absolute ...
Acute: Hematuria, azotemia. Chronic: Serum creatinine ,1.5 mg/dL, proteinuria ,1+ on dipstick. ...
Azotemia, Uremia, Acute Tubular Necrosis, Acute Intrinsic Renal Failure. ... Aka: Acute Kidney Injury, Acute Renal Failure, Acute Renal Insufficiency, Renal Failure, Azotemia, Uremia, Acute Tubular ... Azotemia. *Accumulation of nitrogen waste products in the blood (Blood Urea Nitrogen) ...
Azotemia * Bartter Syndrome * BK Virus Nephropathy * Cardiorenal Syndrome * Chronic Kidney Disease (CKD) ...
Furosemide can cause dehydration and azotemia. If increasing azotemia and oliguria occur during treatment of severe progressive ...
Withhold in patients with dehydration and/or prerenal azotemia.. Iodinated contrast imaging procedures. ...
Only 1 dog developed azotemia. Serum alanine aminotransferase activity increased in some dogs but decreased when treatment was ...
Nesiritide may also affect renal function and cause azotemia in patients with severe heart failure. Nesiritide may also affect ... renal function and cause azotemia in patients with severe heart failure whose renal function is dependent on the activity of ...
Azotemia, and hyperbilirubinemia are more prominent. Aminotranferases (liver enzymes) become elevated. When respiratory muscles ... Kidneys (acute renal failure): oliguria, anuria, azotemia, proteinuria Liver- elevated levels of serum bilirubin, alkaline ...
Furosemide can cause dehydration and azotemia. If increasing azotemia and oliguria occur during treatment of severe progressive ...

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