Azotemia is an elevation of blood urea nitrogen (BUN) and serum creatinine levels.

The reference range for BUN is 8-20 mg/dL, and the normal range for serum creatinine is 0.7-1.4 mg/dL. Each human kidney contains approximately 1 million functional units known as nephrons, which are primarily involved in urine formation. Urine formation ensures that the body eliminates the final products of metabolic activities and excess water in an attempt to maintain a constant internal environment (homeostasis). Urine formation by each nephron involves 3 main processes, as follows: Filtration at the glomerular level Selective reabsorption from the filtrate passing along the renal tubules Secretion by the cells of the tubules into this filtrate Perturbation of any of these processes impairs the kidneys excretory function, resulting in azotemia. The quantity of glomerular filtrate produced each minute by all nephrons in both kidneys is referred to as the glomerular filtration rate (GFR). On average, the GFR is about 125 mL/min (10% less for women), or 180 L/day. About 99% of the filtrate (178 L/day) is reabsorbed, and the rest (2 L/day) is excreted. Measurement of renal function Radionuclide assessment of the GFR is the best available test for measuring kidney function. However, this test is expensive and not widely available, and as a result, serum creatinine concentration and creatinine clearance (CrCl) more commonly are used to estimate GFR. An inverse relation between serum creatinine and the GFR exists; however, serum creatinine and CrCl are not sensitive measures of kidney damage, for 2 reasons. First, substantial renal damage can take place before any decrease in the GFR occurs. Second, a substantial decline in the GFR may lead to only a slight elevation in serum creatinine (see the image below). Because of compensatory hypertrophy and hyperfiltration of the remaining healthy nephrons, an elevation in serum creatinine is apparent only when the GFR falls to about 60-70 mL/min. Acute kidney injury (AKI), previously called acute renal failure (ARF), function. Its causes are numerous and include low blood volume from any cause, exposure tosubstances harmful to the kidney, and obstruction of the urinary tract. AKI is diagnosed on the basis of characteristic laboratory findings, such as elevated blood urea nitrogen andcreatinine, or inability of the kidneys to produce sufficient amounts of urine. AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, and effects to other organ systems. Management includes supportive care, such as renal replacement therapy, as well as treatment of the underlying disorder. Signs and symptoms[edit] The symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue, loss of appetite, headache, nausea and vomiting.
[3] [1][2]

is a rapid loss of kidney

Marked increases in the potassium level can lead

to irregularities in the heartbeat, which can be severe and life-threatening. affected, though hypertension is rare.
[5]

[4]

Fluid balance is frequently

Pain in the flanks may be encountered in some conditions (such as thrombosis of the renal blood vessels or inflammation of the kidney); this is the result of stretching of the fibrous tissue capsule surrounding the kidney.
[6]

If the kidney injury is the result of dehydration, there may be thirst as well as evidence of fluid
[6]

depletion on physical examination.

Physical examination may also provide other clues as to the

[6]

underlying cause of the kidney problem, such as a rash in interstitial nephritis and a palpable bladder.

Inability to excrete sufficient fluid from the body can cause accumulation of fluid in the limbs (peripheral edema) and the lungs (pulmonary edema), as well as cardiac tamponade as a result of fluid effusions. Causes[edit] AKI can be caused by disease, crush injury, contrast agents, some antibiotics, and more. The causes of acute kidney injury are commonly categorized into prerenal, intrinsic, and postrenal.
[3] [5]

Classic laboratory findings in AKI

Type

UOsm UNa FeNa

BUN/Cr

Prerenal >500 <10 <1%

>20

Intrinsic <350 >20 >2% <15

[citation needed]

Postrenal <350 >40 >4% Prerenal[edit]

>15

Prerenal causes of AKI ("pre-renal azotemia") are those that decrease effective blood flow to the kidney. These include systemic causes, such as low blood volume, low blood pressure, heart failure, and local changes to the blood vessels supplying the kidney. The latter include renal artery stenosis, or the narrowing of the renal arterywhich supplies the kidney with blood, and renal vein thrombosis, which is the formation of a blood clot in the renal vein that drains blood from the kidney.

Renal ischaemia ultimately results in functional disorder, depression of GFR, or both. These causes stem from the inadequate cardiac output and hypovolemia or vascular diseases causing reduced perfusion of both kidneys. Both kidneys need to be affected as one kidney is still more than adequate for normal kidney function. Intrinsic[edit] Sources of damage to the kidney itself are dubbed intrinsic. Intrinsic AKI can be due to damage to the glomeruli, renal tubules, orinterstitium. Common causes of each are glomerulonephritis, acute tubular necrosis (ATN), and acute interstitial nephritis (AIN), respectively. A cause of intrinsic acute renal failure is tumor lysis syndrome. Postrenal[edit] Postrenal AKI is a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasia, kidney stones, obstructed urinary catheter, bladder stone, bladder, ureteral or renal malignancy. It is useful to perform a bladder scan or a post void residual to rule out urinary retention. In post void residual, a catheter is inserted immediately after urinating to measure fluid still in the bladder. 50-100ml suggests neurogenic bladder. A renal ultrasound will demonstrate hydronephrosis if present. A CT scan of the abdomen will also demonstrate bladder distension or hydronephrosis, however, in case of acute renal failure, the use of IV contrast is contraindicated. On the basic metabolic panel, the ratio of BUN to creatinine may indicate post renal failure. Diagnosis[edit] Detection[edit] The deterioration of renal function may be discovered by a measured decrease in urine output. Often, it is diagnosed on the basis ofblood tests for substances normally eliminated by the kidney: urea and creatinine. Both tests have their disadvantages. For instance, it takes about 24 hours for the creatinine level to rise, even if both kidneys have ceased to function. A number of alternative markers has been proposed (such as NGAL, KIM-1, IL18 and cystatin C), but none are currently established enough to replace creatinine as a marker of renal function.
[citation needed][when?] [7]

Sodium and potassium, two electrolytes that are commonly deranged in people with acute kidney injury, are typically measured together with urea and creatinine. Further testing[edit] Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. These may include urine sediment analysis, renal ultrasound and/or kidney biopsy. Indications for renal biopsy in the setting of AKI include:
[8] [citation needed]

1. Unexplained AKI 2. AKI in the presence of the nephritic syndrome 3. Systemic disease associated with AKI Classification[edit] Acute kidney injury is diagnosed on the basis of clinical history and laboratory data. A diagnosis is made when there is rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria. Definition[edit] Introduced by the Acute Kidney Injury Network (AKIN), specific criteria exist for the diagnosis of AKI: 1. Rapid time course (less than 48 hours) 2. Reduction of kidney function Rise in serum creatinine, defined by either: Absolute increase in serum creatinine of 0.3 mg/dl (26.4 mol/l) Percentage increase in serum creatinine of 50%
[9]

Reduction in urine output, defined as <0.5 ml/kg/hr for more than 6 hours

Staging[edit] The RIFLE criteria, proposed by the Acute Dialysis Quality Initiative (ADQI) group, aid in the staging of patients with AKI:
[10][11]

Risk: GFR decrease >25%, serum creatinine increased 1.5 times or urine production of <0.5 ml/kg/hr for 6 hours

Injury: GFR decrease >50%, doubling of creatinine or urine production <0.5 ml/kg/hr for 12 hours Failure: GFR decrease >75%, tripling of creatinine or creatinine >355 mol/ l (with a rise of >44) (>4 mg/dl) OR urine output below 0.3 ml/kg/hr for 24 hours

Loss: persistent AKI or complete loss of kidney function for more than 4 weeks End-stage renal disease: need for renal replacement therapy (RRT) for more than 3 months

Treatment[edit] The management of AKI hinges on identification and treatment of the underlying cause. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances.
[12]

Monitoring of renal function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate. Specific therapies[edit] In prerenal AKI without fluid overload, administration of intravenous fluids is typically the first step to improve renal function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid. Should low blood pressure prove a persistent problem in the fluid-replete patient, inotropes such as norepinephrine and dobutamine may be given to improve cardiac output and hence renal perfusion. While a useful pressor, there is no evidence to suggest that dopamine is of any specific benefit, may be harmful. The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to Wegener's granulomatosis may respond to steroid medication. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as aminoglycoside,penicillin, NSAIDs, or paracetamol.
[6] [13]

and

If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary. Diuretic agents[edit] The use of diuretics such as furosemide, is widespread and sometimes convenient in ameliorating fluid overload, and is not associated with higher mortality (risk of death). Renal replacement therapy[edit] Renal replacement therapy, such as with hemodialysis, may be instituted in some cases of AKI. A systematic review of the literature in 2008 demonstrated no difference in outcomes between the use of intermittent hemodialysis and continuous venovenous hemofiltration(CVVH).
[12][16] [15] [14]

Among critically ill

patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis. Complications[edit] Metabolic acidosis, hyperkalemia, and pulmonary edema bicarbonate, antihyperkalemic measures, and diuretics. Lack of improvement with fluid resuscitation, therapy-resistant hyperkalemia, metabolic acidosis, or fluid overload may necessitateartificial support in the form of dialysis or hemofiltration.
[4] [17]

may require medical treatment with sodium

Prognosis[edit] Depending on the cause, a proportion of patients will never regain full renal function, thus entering endstage renal failure and requiring lifelong dialysis or a kidney transplant. Patients with AKI are more likely to die prematurely after they were discharged from hospital even if their kidney function has recovered. Epidemiology[edit] Acute kidney injury is common among hospitalized patients. It affects some 3-7% of patients admitted to the hospital and approximately 25-30% of patients in the intensive care unit.
[18] [2]

Diabetic nephropathy occurs in type 1 (formerly called insulin-dependent or juvenile onset) and type 2 (formerly called non-insulin-dependent or adult onset) diabetes mellitus, and in other secondary forms of diabetes mellitus, for example after pancreatitis or pancreatectomy, in which duration of diabetes is longenough and level of glycemia high enough to result in complications. The following data concerning the epidemiology of renal disease may not represent the current clinical course of the disease. Some of the evidence was obtained before the availability of data supporting the efficacy of tight glycemic control, aggressive blood pressure and lipid control, and the specific benefit of angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs). This topic provides an overview of the major nontreatment issues in diabetic nephropathy. The treatment of diabetic nephropathy is discussed separately. CLINICAL FEATURES Diabetic kidney disease is a glomerulopathy defined by characteristic structural and functional changes. The predominant structural changes include mesangial expansion, glomerular basement membrane thickening, and glomerular sclerosis. The major clinical manifestations of diabetic nephropathy are albuminuria, less often hematuria, and, in many patients, progressive chronic kidney disease, which can be slowed or prevented with optimal therapy. This review will address the treatment of diabetic nephropathy, particularly the importance of glycemic control and of rigorous antihypertensive therapy, with emphasis on the use of angiotensin converting enzyme inhibitors or angiotensin II receptor blockers. In addition to data from controlled trials, further proof of benefit from these therapies is the observation that the incidence of end-stage renal disease among patients with type 1 diabetes may be decreasing

Classification: Antibiotic, Quinolones Action: Semisynthetic antibacterial agent that inhibits bacterial DNA gyrase, necessary for supercoiling (conversion of intermediate fragments into highmolecular weight DNA) of the DNA, thereby preventing DNA replication, transcription, repair and recombination i susceptible bacteria. Indication: Infections caused by susceptible strains of microorganisms in acute maxillary sinusitis, acute bacterial exacerbation of chronic bronchitis, community-acquired pneumonia, nosocomial pneumonia, uncomplicated skin and skin structure infections, complicated and uncomplicated urinary tract infection (UTI) and acute pyelonephritis. Adverse Reactions: Nausea, diarrhea, headache, dizziness, insomnia, musculoskeletal effects, pain, reddening of the infusion site, phlebitis, increase in liver enzymes, eosinophilia, leukopenia, asthenia, fungal overgrowth and proliferation of other resistant microorganisms. Eye irritation, eyelid itching, shocklike symptoms. Hypersensitivity, corneal lesion. Nursing Considerations Assessment Obtain baseline assessment of patient signs and symptoms of infections and reassess during treatment: characteristics of wound, sputum, urine, stool, fever and WBC count (> 10,000/ mm) Obtain C&S before starting drug therapy to identify if correct treatment has been initiated. Assess patient for previous sensitivity reaction and reassess for allergic an anaphylactic reaction during therapy: rash, urticaria, pruritus, chills, fever, joint paint. (Epinephrine and resuscitation equipment must be available for anaphylactic reaction) Obtain history of seizure disorder or other CNS disease before initiating therapy Monitor for possible drug induced adverse reactions Assess hematologic status: bleeding, ecchymosis, bleeding gums, hematuria, and stool guaiac. Monitor CBC, Hgb, Hct Assess renal function: urine output. Monitor BUN, creatinine, serum electrolytes: potassium, sodium, chloride. Assess liver function: jaundice, clay colored stools. Monitor: AST, ALT, LDH,bilirubin, alkaline phosphatase and Coombs test monthly if patient is on long-term therapy. Assess bowel pattern: if severe diarrhea occurs, drug should be discontinued. Assess for overgrowth of infection: perineal itching, fever, malaise, redness, pain, swelling, drainage, rash, diarrhea, change in cough, sputum. Assess patients and familys knowledge of drug therapy.

Planning Give oral administration 4 hours before or 2 hours after antacids, iron, calcium, zinc Check for irritation, extravasation, phlebitis daily

Implementation Instruct patient to continue taking drug as prescribed for the length of time ordered, even if felling better and to avoid taking other medications unless approved by physician. Advice patient to take drug with plenty of fluids, at least 2 L/day and to avoid antacids, sucralfate and products containing iron or zinc for at least 2 hours before and after each dose. Inform patient that toxicity may result if drug is used with theophylline. Contact physician before using theophylline with this drug. Warn patient to avoid hazardous tasks and activities requiring alertnessuntil CNS effects are known. The drug must be taken around the clock to maintain blood levels. Teach patient to report: sore throat, bruising, bleeding, joint pain, vaginal itching, loose foul-smelling stools, furry tongue, itching, rash, pruritus, urticaria, diarrhea with blood or pus and other adverse reactions. Instruct diabetic patients to monitor glucose levels, a hypoglycemic reaction may indicate need to stop medication. Instruct patient to rinse mouth frequently and use sugarless coated candy or gum for dry mouth. Advise patient to avoid sun exposure or use sunscreen to prevent phototoxicity.

Evaluation Absence of signs and symptoms of infection (WBC < 10,000 mm, temp within normal level) Reported improvement in symptoms of infection Absence of drug induced adverse reactions. Patient and family state understanding of drug therapy.

Vastarel Brand Name: Vastarel MR Generic Name: Trimetazidine dihydrochloride Manufacturer: Servier PRESENTATION AND COMPOSITION Boxes of 10 and 60 modified release film-coated tablets dosed at 35 mg of trimetazidine dihydrochloride. Excipients. q.s.f. one tablet. THERAPEUTIC INDICATIONS This drug is recommended in:

Preventive treatment for episodes of angina pectoris (Chronic stable angina). Adjuvant symptomatic treatment for vertigo and tinnitus (noises detected by the ear whistling, which do not correspond to any exterior sounds). Adjuvant treatment of visual disorders of a circulatory origin. CONTRAINDICATIONS Do not take Vastarel MR if you are allergic to any of the constituents. This drug is generally not recommended during breast feeding

buzzing,

SPECIAL WARNINGS AND PRECAUTIONS This drug is not a curative treatment for angina attacks, nor an initial treatment for unstable angina pectoris. It is not a treatment for myocardial infarction. In the event of an angina attack, inform your doctor. Tests may be required and your treatment may possibly be modified. SIDE EFFECTS As with all drugs, Vastarel MR is likely to have undesirable effects: Rare cases of gastro-intestinal disorders (nausea, vomiting) It you notice any undesirable effects, which have not been mentioned here, you should inform your doctor or pharmacist. PREGNANCY AND BREASTFEEDING Pregnancy It is preferable not to take this medicine during pregnancy, if you discover that you are pregnant whilst taking this medicine, consult your doctor as he alone can judge the necessity of continuing your treatment Breastfeeding In the absence of data on excretion in breast milk, breastfeeding is not recommended during treatment. Ask your doctor or pharmacist's advice before taking any medicine. DOSAGE AND METHOD OF ADMINISTRATION Oral route. The usual dosage is 1 tablet in the morning and evening. Tablets should be swallowed with a glass of water at meal times. If you think that the effect of Vastarel MR is too strong or too weak, talk to your doctor or pharmacist. OVERDOSAGE Consult a doctor or a pharmacist immediately. WHAT TO DO IN CASE ONE OR SEVERAL DOSES HAVE BEEN MISSED Resume treatment normally. Do not take a double dose to compensate for the single dose that you forgot to take. STORAGE CONDITIONS Keep out of the reach and sight of children. Do not use after the expiry date indicated on the box. Trimetazidine inhibits beta-oxidation of fatty acids by blocking long-chain 3-ketoacyl-CoA thiolase, which [6] enhances glucose oxidation. In an ischaemic cell, energy obtained during glucose oxidation requires less oxygen consumption than in the beta-oxidation process. Potentiation of glucose oxidation optimizes

cellular energy processes, thereby maintaining proper energy metabolism during ischaemia. By preserving energy metabolism in cells exposed to hypoxia or ischaemia, trimetazidine prevents a decrease in intracellular ATP levels, thereby ensuring the proper functioning of ionic pumps and [5] transmembrane sodium-potassium flow whilst maintaining cellular homeostasis. PANTOLOC Generic name Pantoprazole Sodium Classification antacids and antiulcerants Indications Symptomatic treatment of mild reflux esophagitis; long term management and prevention of relapse of reflux esophagitis; duodenal and gastric ulcers, reflux esophagitis; eradication of H. pylori. Action Inhibits proton pump activity by binding to hydrogen-potassium adenosine triphosphatase, located at secretory surface of gastric parietal cells, to suppress gastric acid secretion. Adverse Frequently: headache, Rarely: nausea, upper abdominal pain, flatulence, skin rash, pruritus or dizziness. Nursing Considerations alert: dont confuse with protonix tablet, prisolec, prozac, or prevacid drug can be given without regard to meals drug shouldnt be used for maintenance therapy beyond 16 weeks. symptomatic response to therapy doent preclude the presence of gastric malignancy. reactions diarrhea

Quetiapine is an antipsychotic medicine. It works by changing the actions of chemicals in the brain. Quetiapine is used to treat schizophrenia in adults and children who are at least 13 years old. Quetiapine is used to treat bipolar disorder (manic depression) in adults and children who are at least 10 years old. Quetiapine is also used together with antidepressant medications to treat major depressive disorder in adults. Quetiapine may also be used for purposes not listed in this medication guide.

Seroquel 100 mg

round, yellow, imprinted with SEROQUEL 100 What are the possible side effects of quetiapine (Seroquel, Seroquel XR)? Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat. Call your doctor at once if you have any new or worsening symptoms such as: mood or behavior changes,anxiety, panic attacks, trouble sleeping, or if you feel impulsive, irritable, agitated, hostile, aggressive, restless, hyperactive (mentally or physically), more depressed, or have thoughts about suicide or hurting yourself. Stop using quetiapine and call your doctor at once if you have a serious side effect such as: very stiff (rigid) muscles, high fever, sweating, confusion, fast or uneven heartbeats, tremors; feeling like you might pass out; jerky muscle movements you cannot control, trouble swallowing, problems with speech; tremors, or restless muscle movements in your eyes, tongue, jaw, neck, arms, or legs; mask-like appearance of the face, trouble swallowing, problems with speech; blurred vision, eye pain, or seeing halos around lights; increased thirst and urination, excessive hunger, fruity breath odor, weakness, nausea and vomiting; or fever, chills, body aches, flu symptoms, white patches or sores inside your mouth or on your lips. Less serious side effects may include: dizziness, drowsiness, tired feeling; dry mouth, sore throat; stomach pain, upset stomach, nausea, vomiting, constipation; breast swelling or discharge; missed menstrual periods; or increased appetite, weight gain. This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088. What is the most important information I should know about quetiapine (Seroquel, Seroquel XR)?

Quetiapine is not for use in psychotic conditions related to dementia. Quetiapine may cause heart failure, sudden death, or pneumonia in older adults with dementia-related conditions. Stop using quetiapine and call your doctor at once if you have the following symptoms: very stiff (rigid) muscles, high fever, sweating, confusion, fast or uneven heartbeats, tremors, uncontrolled muscle movements, feeling light-headed, blurred vision, eye pain, increased thirst and urination, excessive hunger, fruity breath odor, weakness, nausea and vomiting. Report any new or worsening symptoms to your doctor, such as: mood or behavior changes, anxiety, panic attacks, trouble sleeping, or if you feel impulsive, irritable, agitated, hostile, aggressive, restless, hyperactive (mentally or physically), more depressed, or have thoughts about suicide or hurting yourself.