Azotemia
Uremia
Blood Urea Nitrogen
Acute Kidney Injury
Hypoaldosteronism
Kidney Tubular Necrosis, Acute
Kidney
Kidney Failure, Chronic
Pancreatitis
Cats
Click Chemistry
Pancreatitis, Chronic
Pancreatitis, Acute Necrotizing
Pancreatitis, Alcoholic
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)
(+info)Treatment for uremia typically involves dialysis or kidney transplantation to remove excess urea from the blood and restore normal kidney function. In some cases, medications may be prescribed to help manage symptoms such as high blood pressure, anemia, or electrolyte imbalances.
The term "uremia" is derived from the Greek words "oura," meaning "urea," and "emia," meaning "in the blood." It was first used in the medical literature in the late 19th century to describe a condition caused by excess urea in the blood. Today, it remains an important diagnostic term in nephrology and is often used interchangeably with the term "uremic syndrome."
The definition of AKI has evolved over time, and it is now defined as a syndrome characterized by an abrupt or rapid decrease in kidney function, with or without oliguria (decreased urine production), and with evidence of tubular injury. The RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria are commonly used to diagnose and stage AKI based on serum creatinine levels, urine output, and other markers of kidney damage.
There are three stages of AKI, with stage 1 representing mild injury and stage 3 representing severe and potentially life-threatening injury. Treatment of AKI typically involves addressing the underlying cause, correcting fluid and electrolyte imbalances, and providing supportive care to maintain blood pressure and oxygenation. In some cases, dialysis may be necessary to remove waste products from the blood.
Early detection and treatment of AKI are crucial to prevent long-term damage to the kidneys and improve outcomes for patients.
There are several possible causes of hypoaldosteronism, including:
1. Adrenal gland disorders: Damage to the adrenal glands, such as from injury or infection, can lead to a decrease in aldosterone production.
2. Genetic mutations: Some people may be born with genetic mutations that affect the production of aldosterone.
3. Autoimmune disorders: In some cases, the immune system may attack the adrenal glands and disrupt aldosterone production.
4. Medications: Certain medications, such as steroids and diuretics, can suppress the production of aldosterone.
5. Primary aldosteronism: This is a condition where the adrenal glands produce too much aldosterone, leading to an imbalance in electrolytes and fluids.
Treatment for hypoaldosteronism will depend on the underlying cause of the condition. In some cases, medications such as salt substitutes or diuretics may be prescribed to help manage symptoms. In other cases, hormone replacement therapy may be necessary to replace the missing aldosterone.
It is important to note that hypoaldosteronism can lead to more serious complications if left untreated, such as dehydration, electrolyte imbalances, and heart arrhythmias. If you suspect you may have hypoaldosteronism, it is important to consult with a healthcare professional for proper diagnosis and treatment.
In this answer, we will explore the definition of 'Kidney Tubular Necrosis, Acute' in more detail, including its causes, symptoms, diagnosis, and treatment options.
What is Kidney Tubular Necrosis, Acute?
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Kidney Tubular Necrosis, Acute (ATN) is a condition that affects the tubules of the kidneys, leading to inflammation and damage. The condition is often caused by various factors such as sepsis, shock, toxins, or medications.
The term "acute" refers to the sudden and severe nature of the condition, which can progress rapidly within hours or days. The condition can be life-threatening if left untreated, and it is important to seek medical attention immediately if symptoms persist or worsen over time.
Causes of Kidney Tubular Necrosis, Acute
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There are various factors that can cause Kidney Tubular Necrosis, Acute, including:
### 1. Sepsis
Sepsis is a systemic inflammatory response to an infection, which can lead to damage to the tubules of the kidneys.
### 2. Shock
Shock can cause a decrease in blood flow to the kidneys, leading to damage and inflammation.
### 3. Toxins
Exposure to certain toxins, such as heavy metals or certain medications, can damage the tubules of the kidneys.
### 4. Medications
Certain medications, such as antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs), can cause damage to the tubules of the kidneys.
### 5. Infection
Infections such as pyelonephritis or perinephric abscess can spread to the kidneys and cause inflammation and damage to the tubules.
### 6. Radiation necrosis
Radiation therapy can cause damage to the kidneys, leading to inflammation and scarring.
### 7. Kidney transplant rejection
Rejection of a kidney transplant can lead to inflammation and damage to the tubules of the transplanted kidney.
Symptoms of Kidney Tubular Necrosis, Acute
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The symptoms of acute tubular necrosis can vary depending on the severity of the condition and the underlying cause. Some common symptoms include:
### 1. Fatigue
Fatigue is a common symptom of acute tubular necrosis, as the condition can lead to a decrease in the kidneys' ability to filter waste products from the blood.
### 2. Nausea and vomiting
Nausea and vomiting can occur due to electrolyte imbalances and changes in fluid levels in the body.
### 3. Decreased urine output
Acute tubular necrosis can cause a decrease in urine production, as the damaged tubules are unable to filter waste products from the blood effectively.
### 4. Swelling (edema)
Swelling in the legs, ankles, and feet can occur due to fluid buildup in the body.
### 5. Abdominal pain
Abdominal pain can be a symptom of acute tubular necrosis, as the condition can cause inflammation and scarring in the kidneys.
### 6. Fever
Fever can occur due to infection or inflammation in the kidneys.
### 7. Blood in urine (hematuria)
Hematuria, or blood in the urine, can be a symptom of acute tubular necrosis, as the damaged tubules can leak blood into the urine.
## Causes and risk factors
The exact cause of acute tubular necrosis is not fully understood, but it is believed to be due to damage to the kidney tubules, which can occur for a variety of reasons. Some possible causes and risk factors include:
1. Sepsis: Bacterial infections can spread to the kidneys and cause inflammation and damage to the tubules.
2. Toxins: Exposure to certain toxins, such as heavy metals or certain medications, can damage the kidney tubules.
3. Medications: Certain medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics, can cause kidney damage and increase the risk of acute tubular necrosis.
4. Hypotension: Low blood pressure can reduce blood flow to the kidneys and increase the risk of acute tubular necrosis.
5. Shock: Severe shock can lead to damage to the kidney tubules.
6. Burns: Severe burns can cause damage to the kidneys and increase the risk of acute tubular necrosis.
7. Trauma: Traumatic injuries, such as those caused by car accidents or falls, can damage the kidneys and increase the risk of acute tubular necrosis.
8. Surgery: Major surgery can cause damage to the kidneys and increase the risk of acute tubular necrosis.
9. Kidney disease: People with pre-existing kidney disease are at increased risk of developing acute tubular necrosis.
10. Chronic conditions: Certain chronic conditions, such as diabetes and high blood pressure, can increase the risk of developing acute tubular necrosis.
It is important to note that acute tubular necrosis can occur in people with no underlying medical conditions or risk factors, and it is often a diagnosis of exclusion, meaning that other potential causes of the person's symptoms must be ruled out before the diagnosis can be made.
Proteinuria is usually diagnosed by a urine protein-to-creatinine ratio (P/C ratio) or a 24-hour urine protein collection. The amount and duration of proteinuria can help distinguish between different underlying causes and predict prognosis.
Proteinuria can have significant clinical implications, as it is associated with increased risk of cardiovascular disease, kidney damage, and malnutrition. Treatment of the underlying cause can help reduce or eliminate proteinuria.
A condition in which the kidneys gradually lose their function over time, leading to the accumulation of waste products in the body. Also known as chronic kidney disease (CKD).
Prevalence:
Chronic kidney failure affects approximately 20 million people worldwide and is a major public health concern. In the United States, it is estimated that 1 in 5 adults has CKD, with African Americans being disproportionately affected.
Causes:
The causes of chronic kidney failure are numerous and include:
1. Diabetes: High blood sugar levels can damage the kidneys over time.
2. Hypertension: Uncontrolled high blood pressure can cause damage to the blood vessels in the kidneys.
3. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste and excess fluids from the blood.
4. Interstitial nephritis: Inflammation of the tissue between the kidney tubules.
5. Pyelonephritis: Infection of the kidneys, usually caused by bacteria or viruses.
6. Polycystic kidney disease: A genetic disorder that causes cysts to grow on the kidneys.
7. Obesity: Excess weight can increase blood pressure and strain on the kidneys.
8. Family history: A family history of kidney disease increases the risk of developing chronic kidney failure.
Symptoms:
Early stages of chronic kidney failure may not cause any symptoms, but as the disease progresses, symptoms can include:
1. Fatigue: Feeling tired or weak.
2. Swelling: In the legs, ankles, and feet.
3. Nausea and vomiting: Due to the buildup of waste products in the body.
4. Poor appetite: Loss of interest in food.
5. Difficulty concentrating: Cognitive impairment due to the buildup of waste products in the brain.
6. Shortness of breath: Due to fluid buildup in the lungs.
7. Pain: In the back, flank, or abdomen.
8. Urination changes: Decreased urine production, dark-colored urine, or blood in the urine.
9. Heart problems: Chronic kidney failure can increase the risk of heart disease and heart attack.
Diagnosis:
Chronic kidney failure is typically diagnosed based on a combination of physical examination findings, medical history, laboratory tests, and imaging studies. Laboratory tests may include:
1. Blood urea nitrogen (BUN) and creatinine: Waste products in the blood that increase with decreased kidney function.
2. Electrolyte levels: Imbalances in electrolytes such as sodium, potassium, and phosphorus can indicate kidney dysfunction.
3. Kidney function tests: Measurement of glomerular filtration rate (GFR) to determine the level of kidney function.
4. Urinalysis: Examination of urine for protein, blood, or white blood cells.
Imaging studies may include:
1. Ultrasound: To assess the size and shape of the kidneys, detect any blockages, and identify any other abnormalities.
2. Computed tomography (CT) scan: To provide detailed images of the kidneys and detect any obstructions or abscesses.
3. Magnetic resonance imaging (MRI): To evaluate the kidneys and detect any damage or scarring.
Treatment:
Treatment for chronic kidney failure depends on the underlying cause and the severity of the disease. The goals of treatment are to slow progression of the disease, manage symptoms, and improve quality of life. Treatment may include:
1. Medications: To control high blood pressure, lower cholesterol levels, reduce proteinuria, and manage anemia.
2. Diet: A healthy diet that limits protein intake, controls salt and water intake, and emphasizes low-fat dairy products, fruits, and vegetables.
3. Fluid management: Monitoring and control of fluid intake to prevent fluid buildup in the body.
4. Dialysis: A machine that filters waste products from the blood when the kidneys are no longer able to do so.
5. Transplantation: A kidney transplant may be considered for some patients with advanced chronic kidney failure.
Complications:
Chronic kidney failure can lead to several complications, including:
1. Heart disease: High blood pressure and anemia can increase the risk of heart disease.
2. Anemia: A decrease in red blood cells can cause fatigue, weakness, and shortness of breath.
3. Bone disease: A disorder that can lead to bone pain, weakness, and an increased risk of fractures.
4. Electrolyte imbalance: Imbalances of electrolytes such as potassium, phosphorus, and sodium can cause muscle weakness, heart arrhythmias, and other complications.
5. Infections: A decrease in immune function can increase the risk of infections.
6. Nutritional deficiencies: Poor appetite, nausea, and vomiting can lead to malnutrition and nutrient deficiencies.
7. Cardiovascular disease: High blood pressure, anemia, and other complications can increase the risk of cardiovascular disease.
8. Pain: Chronic kidney failure can cause pain, particularly in the back, flank, and abdomen.
9. Sleep disorders: Insomnia, sleep apnea, and restless leg syndrome are common complications.
10. Depression and anxiety: The emotional burden of chronic kidney failure can lead to depression and anxiety.
Types of Kidney Diseases:
1. Acute Kidney Injury (AKI): A sudden and reversible loss of kidney function that can be caused by a variety of factors, such as injury, infection, or medication.
2. Chronic Kidney Disease (CKD): A gradual and irreversible loss of kidney function that can lead to end-stage renal disease (ESRD).
3. End-Stage Renal Disease (ESRD): A severe and irreversible form of CKD that requires dialysis or a kidney transplant.
4. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste products.
5. Interstitial Nephritis: An inflammation of the tissue between the tubules and blood vessels in the kidneys.
6. Kidney Stone Disease: A condition where small, hard mineral deposits form in the kidneys and can cause pain, bleeding, and other complications.
7. Pyelonephritis: An infection of the kidneys that can cause inflammation, damage to the tissues, and scarring.
8. Renal Cell Carcinoma: A type of cancer that originates in the cells of the kidney.
9. Hemolytic Uremic Syndrome (HUS): A condition where the immune system attacks the platelets and red blood cells, leading to anemia, low platelet count, and damage to the kidneys.
Symptoms of Kidney Diseases:
1. Blood in urine or hematuria
2. Proteinuria (excess protein in urine)
3. Reduced kidney function or renal insufficiency
4. Swelling in the legs, ankles, and feet (edema)
5. Fatigue and weakness
6. Nausea and vomiting
7. Abdominal pain
8. Frequent urination or polyuria
9. Increased thirst and drinking (polydipsia)
10. Weight loss
Diagnosis of Kidney Diseases:
1. Physical examination
2. Medical history
3. Urinalysis (test of urine)
4. Blood tests (e.g., creatinine, urea, electrolytes)
5. Imaging studies (e.g., X-rays, CT scans, ultrasound)
6. Kidney biopsy
7. Other specialized tests (e.g., 24-hour urinary protein collection, kidney function tests)
Treatment of Kidney Diseases:
1. Medications (e.g., diuretics, blood pressure medication, antibiotics)
2. Diet and lifestyle changes (e.g., low salt intake, increased water intake, physical activity)
3. Dialysis (filtering waste products from the blood when the kidneys are not functioning properly)
4. Kidney transplantation ( replacing a diseased kidney with a healthy one)
5. Other specialized treatments (e.g., plasmapheresis, hemodialysis)
Prevention of Kidney Diseases:
1. Maintaining a healthy diet and lifestyle
2. Monitoring blood pressure and blood sugar levels
3. Avoiding harmful substances (e.g., tobacco, excessive alcohol consumption)
4. Managing underlying medical conditions (e.g., diabetes, high blood pressure)
5. Getting regular check-ups and screenings
Early detection and treatment of kidney diseases can help prevent or slow the progression of the disease, reducing the risk of complications and improving quality of life. It is important to be aware of the signs and symptoms of kidney diseases and seek medical attention if they are present.
There are several causes of pancreatitis, including:
1. Gallstones: These can block the pancreatic duct, causing inflammation.
2. Alcohol consumption: Heavy alcohol use can damage the pancreas and lead to inflammation.
3. High triglycerides: Elevated levels of triglycerides in the blood can cause pancreatitis.
4. Infections: Viral or bacterial infections can infect the pancreas and cause inflammation.
5. Genetic factors: Some people may be more susceptible to pancreatitis due to inherited genetic mutations.
6. Pancreatic trauma: Physical injury to the pancreas can cause inflammation.
7. Certain medications: Some medications, such as certain antibiotics and chemotherapy drugs, can cause pancreatitis as a side effect.
Symptoms of pancreatitis may include:
1. Abdominal pain
2. Nausea and vomiting
3. Fever
4. Diarrhea or bloating
5. Weight loss
6. Loss of appetite
Treatment for pancreatitis depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to manage symptoms and address any complications. Treatment options may include:
1. Pain management: Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) or opioids may be used to manage abdominal pain.
2. Fluid replacement: Intravenous fluids may be given to replace lost fluids and electrolytes.
3. Antibiotics: If the pancreatitis is caused by an infection, antibiotics may be prescribed to treat the infection.
4. Nutritional support: Patients with pancreatitis may require nutritional support to ensure they are getting enough calories and nutrients.
5. Pancreatic enzyme replacement therapy: In some cases, pancreatic enzyme replacement therapy may be necessary to help the body digest food.
6. Surgery: In severe cases of pancreatitis, surgery may be necessary to remove damaged tissue or repair damaged blood vessels.
It is important to seek medical attention if you experience persistent abdominal pain or other symptoms of pancreatitis, as early treatment can help prevent complications and improve outcomes.
A persistent inflammation of the pancreas that can last for months or even years, leading to chronic pain, digestive problems, and other complications.
Pancreatitis is a condition where the pancreas becomes inflamed, which can be caused by various factors such as gallstones, alcohol consumption, certain medications, and genetics. Chronic pancreatitis is a type of pancreatitis that persists over time, leading to ongoing symptoms and complications.
The symptoms of chronic pancreatitis can vary but may include abdominal pain, nausea, vomiting, diarrhea, weight loss, and fatigue. The condition can also lead to complications such as infection, bleeding, and narrowing or blockage of the pancreatic ducts.
Chronic pancreatitis is diagnosed through a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment options for chronic pancreatitis may include medications to manage pain and inflammation, lifestyle changes such as avoiding alcohol and fatty foods, and in some cases, surgery to remove the damaged pancreatic tissue.
The prognosis for chronic pancreatitis varies depending on the underlying cause of the condition and the severity of the inflammation. In some cases, the condition can be managed with medication and lifestyle changes, while in others, surgery may be necessary to remove the damaged pancreatic tissue.
Preventing chronic pancreatitis is not always possible, but avoiding risk factors such as alcohol consumption and certain medications can help reduce the likelihood of developing the condition. Early diagnosis and treatment can also improve outcomes for individuals with chronic pancreatitis.
The symptoms of ANP can include:
1. Severe abdominal pain that worsens rapidly within a few days
2. Fever
3. Nausea and vomiting
4. Diarrhea or constipation
5. Blood in stools or vomitus
6. Signs of organ failure, such as decreased blood pressure, tachycardia, and tachypnea
7. Sepsis or infection
8. Pleural effusion or ascites
9. Rhabdomyolysis (breakdown of muscle tissue)
10. Elevated serum levels of inflammatory markers, such as CRP and WBC.
The diagnosis of ANP is based on a combination of clinical features, laboratory tests, and imaging studies. Laboratory tests may include:
1. Elevated serum levels of amylase and lipase
2. Elevated blood urea nitrogen (BUN) and creatinine
3. Increased white blood cell count and elevated C-reactive protein (CRP)
4. Electrolyte imbalance
5. Renal failure
6. Hepatic dysfunction
7. Cardiovascular instability
8. Coagulopathy
9. Hypocalcemia
10. Hyperglycemia
Imaging studies, such as CT scans or MRI, may show:
1. Widespread pancreatic necrosis
2. Inflammation in the surrounding tissues
3. Abscesses or fluid collections in the pancreas or peripancreatic tissues
4. Obstruction of the pancreatic duct
5. Intestinal ischemia or perforation
6. Peritonitis or retroperitoneal abscess
The treatment of ANP involves a multidisciplinary approach, including surgical, medical, and radiological interventions. The goals of treatment are to:
1. Stabilize the patient's vital signs and correct any electrolyte imbalances
2. Manage infection and sepsis
3. Provide supportive care for any organ dysfunction or failure
4. Remove any obstructions or necrotic tissue from the pancreas
5. Promote pancreatic tissue healing and regeneration
6. Prevent further complications, such as pancreatic fibrosis or pseudocyst formation
Surgical interventions may include:
1. Pancreatectomy: removal of the necrotic or infarcted pancreatic tissue
2. Drainage of abscesses or fluid collections
3. Repair of any obstructions in the pancreatic duct
4. Debridement of any infected or necrotic tissue
5. Reconstruction of the pancreas and surrounding tissues
Medical interventions may include:
1. Antibiotics to treat infection and sepsis
2. Pain management with analgesics and sedatives
3. Management of diabetes or other endocrine disorders
4. Supportive care for any organ dysfunction or failure
5. Monitoring of vital signs and laboratory values
Radiological interventions may include:
1. Imaging studies to evaluate the extent of the inflammation and assess the response to treatment
2. Therapeutic interventions, such as endoscopic retrograde cholangiopancreatography (ERCP) or percutaneous drainage of abscesses
The prognosis for ANP depends on several factors, including the severity of the inflammation, the presence of any complications, and the timeliness and effectiveness of treatment. In general, the sooner treatment is initiated, the better the prognosis. Mortality rates for ANP have been reported to range from 5-20%, with higher mortality rates associated with more severe disease and delayed treatment.
Prevention of ANP involves prompt management of any underlying conditions or risk factors that may lead to pancreatitis. This includes:
1. Proper management of gallstones, including cholecystectomy if necessary
2. Treatment of chronic alcoholism and cessation of alcohol consumption
3. Management of hyperlipidemia with appropriate medications and lifestyle modifications
4. Avoiding certain medications that may increase the risk of pancreatitis, such as certain antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs)
5. Maintaining good overall health and avoiding any other potential risk factors for pancreatitis, such as smoking and excessive physical activity.
A type of pancreatitis that is caused by heavy and prolonged alcohol consumption. It is characterized by inflammation of the pancreas that can lead to scarring and impaired pancreatic function. Symptoms include abdominal pain, nausea, vomiting, fever, and diarrhea.
Etiology:
* Heavy and prolonged alcohol consumption (more than 4 drinks per day for men and more than 2 drinks per day for women)
* Binge drinking
* Poor nutrition
* Genetic predisposition
Pathophysiology:
* Alcohol causes pancreatic enzymes to activate prematurely, leading to autodigestion of the pancreas and inflammation
* Inflammation can lead to fibrosis and cirrhosis of the pancreas
* Chronic pancreatitis can lead to exocrine and endocrine insufficiency
Signs and Symptoms:
* Abdominal pain (midline, epigastric)
* Nausea and vomiting
* Fever
* Diarrhea
* Weight loss
* Jaundice
Diagnosis:
* Medical history and physical examination
* Laboratory tests (e.g., lipase, amylase, trypsinogen activation)
* Imaging studies (e.g., CT scan, MRI)
Treatment:
* Alcohol withdrawal and cessation
* Pain management (e.g., nonsteroidal anti-inflammatory drugs [NSAIDs], opioids)
* Nutritional support
* Pancreatic enzyme replacement therapy
* Antibiotics for infected pancreatitis
Prognosis:
* Chronic pancreatitis can lead to long-term impairment of pancreatic function and malnutrition
* Alcoholic pancreatitis is a leading cause of pancreatic cancer
Prevention:
* Avoid heavy and prolonged alcohol consumption
* Follow a healthy diet and lifestyle
Complications:
* Pancreatic cancer
* Chronic pancreatitis
* Pancreatic insufficiency
* Malnutrition
* Infections (e.g., pseudocysts, abscesses)
Epidemiology:
* Alcoholic pancreatitis is the most common form of acute pancreatitis
* The incidence of alcoholic pancreatitis has increased in recent years, possibly due to increased alcohol consumption and improved diagnostic tools
* Chronic pancreatitis affects approximately 5-10% of patients with alcoholic pancreatitis
Etiology:
* Alcohol (ethanol) consumption is the primary risk factor for both acute and chronic pancreatitis
* Other risk factors include gallstones, smoking, obesity, and certain medications (e.g., corticosteroids, NSAIDs)
Pathophysiology:
* Alcohol consumption can damage the pancreatic tissue and trigger an inflammatory response
* The pancreas is a vital organ that produces hormones (insulin, glucagon) and digestive enzymes. Damage to the pancreas can lead to impaired glucose metabolism and malnutrition.
Diagnosis:
* Clinical evaluation (history of alcohol consumption, symptoms, physical examination)
* Laboratory tests (blood tests, lipase levels)
* Imaging studies (CT scan, MRI)
Treatment:
* Supportive care (pain management, fluid replacement)
* Withdrawal of alcohol
* Anti-inflammatory medications (e.g., corticosteroids)
* Pancreatic enzyme replacement therapy
* Surgical intervention (e.g., pancreatectomy, cholecystectomy)
Prognosis:
* Acute pancreatitis has a high mortality rate if left untreated (approximately 20-30%)
* Chronic pancreatitis can lead to long-term morbidity and impaired quality of life
Complications:
* Infection (e.g., pneumonia, sepsis)
* Organ failure (e.g., respiratory, cardiovascular)
* Nutritional deficiencies (e.g., malnutrition, vitamin deficiencies)
* Psychological disorders (e.g., depression, anxiety)
There are several types of vulvar neoplasms, including:
1. Vulvar intraepithelial neoplasia (VIN): This is a precancerous condition that affects the squamous cells on the surface of the vulva. VIN can progress to vulvar cancer if left untreated.
2. Vulvar squamous cell carcinoma: This is the most common type of vulvar cancer and arises from the squamous cells that line the vulva.
3. Vulvar adenocarcinoma: This type of vulvar cancer originates in the glandular cells that are found near the opening of the vagina.
4. Vulvar melanoma: This is a rare type of vulvar cancer that arises from the pigment-producing cells called melanocytes.
5. Lymphoma: This is a type of cancer that affects the immune system and can occur in the vulva.
The symptoms of vulvar neoplasms can vary depending on the type and location of the growth, but may include:
* A visible lump or lesion on the vulva
* Itching, burning, or pain in the affected area
* Discharge or bleeding from the vulva
* Changes in the color or texture of the skin on the vulva
If you suspect you have a vulvar neoplasm, it is important to see a healthcare provider for an accurate diagnosis and treatment. A physical examination and biopsy may be performed to determine the type and extent of the growth. Treatment options will depend on the type and stage of the neoplasm, but may include surgery, radiation therapy, or chemotherapy.
Azotemia
Uremia
Kidney failure
Multiple organ dysfunction syndrome
Asterixis
BUN-to-creatinine ratio
Pierre Grabar
Vitamin D
Cardiorenal syndrome
Urethrostomy
Chronic kidney disease
Kidney ischemia
Epidemic dropsy
Uremic pericarditis
Kidney stone disease
Salmonellosis
Equine proximal enteritis
Salmonella
1962 Tour de France
List of teams and cyclists in the 1962 Tour de France
Comorbidity
Lupus and pregnancy
Milk-alkali syndrome
Pentamidine
Lipocalin-2
Ischemia
Polypeptide antibiotic
Circadian rhythm
Hypoadrenocorticism in dogs
Doxycycline
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- Prerenal azotemia is an abnormally high level of nitrogen waste products in the blood. (medlineplus.gov)
- Prerenal azotemia is common, especially in older adults and in people who are in the hospital. (medlineplus.gov)
- Prerenal azotemia is the most common form of kidney failure in hospitalized people. (medlineplus.gov)
- Conditions in which the heart cannot pump enough blood or pumps blood at a low volume also increase the risk for prerenal azotemia. (medlineplus.gov)
- Prerenal azotemia may have no symptoms. (medlineplus.gov)
- Or, symptoms of the causes of prerenal azotemia may be present. (medlineplus.gov)
- Prerenal azotemia can be reversed if the cause can be found and corrected within 24 hours. (medlineplus.gov)
- Go to the emergency room or call 911 or the local emergency number if you have symptoms of prerenal azotemia. (medlineplus.gov)
- Quickly treating any condition that reduces the volume or force of blood flow through the kidneys may help prevent prerenal azotemia. (medlineplus.gov)
- Profound prerenal azotemia resulting from pyloric stenosis. (bvsalud.org)
Acute renal f1
- Nephrosis can be considered one of the most important toxic effects, due severe intravascular hemolytic disturbance and rhabdomyolysis, along with acute renal failure caused by the toxin components in the tubules and the toxic-isquemic condition, causing azotemia. (ufrgs.br)
Liver enzymes1
- The biochemistry of your dog will be out of whack too, with increased potassium levels, decreased sodium and chlorine levels, increased calcium levels, increased liver enzymes, decreased glucose levels, and azotemia. (dogsnaturallymagazine.com)
Renal failure2
- Inability to concentrate urine does not automatically imply renal disease, just as azotemia does not always imply renal failure. (dvm360.com)
- In other words, isosthenuria + azotemia in these patients does not equal renal failure. (dvm360.com)
Elevation1
- Azotemia is an elevation of blood urea nitrogen (BUN) and serum creatinine levels. (medscape.com)
Dehydration1
- These animals will rapidly develop pre-renal azotemia because of dehydration, but their urine will remain dilute. (dvm360.com)
Clinical1
- Clinical pathology results showed a strong hemolyzed plasma, azotemia, leukocytosis with neutrophilia and monocytosis. (ufrgs.br)
Nitrogen2
- When nitrogen waste products, such as creatinine and urea, build up in the body, the condition is called azotemia. (medlineplus.gov)
- Azotemia is an increase in nitrogen containing compounds in the blood - in particular urea and creatinine. (dogsnaturallymagazine.com)
Function1
- Perturbation of any of these processes impairs the kidney's excretory function, resulting in azotemia. (medscape.com)
