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Monthly Archives: December 2016

Triglycerides and Cholesterol

– Two primary forms of lipids in the blood
– Triglycerides function as energy source and are stored in adipose tissue.
– Cholesterol is primarily used to make steroids hormones, cell membranes.and bile acids.
– Water-insoluble fats that must be bound to apolipoproteins, specialized lipid-carrying proteins
– Lipoprotein is the combination of triglyceride or cholesterol with apolipoprotein

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Lipoproteins

Lipoprotein is the combination of triglyceride or cholesterol with apolipoprotein

– Lipoproteins transport lipids via the blood.

Different types:
– Very-low-density lipoprotein (VLDL)
Produced by the liver
Transports endogenous lipids to the cells

– Low-density lipoprotein (LDL)

– High-density lipoprotein (HDL)
Responsible for “recycling” of cholesterol
Also known as “good cholesterol”

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Cholesterol levels and risk for CHD ( coronary heart disease)

The risk of CHD in patients with cholesterol levels of 300 mg/dL is three to four times greater than that in patients with levels less than 200 mg/dL

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Coronary Heart Disease
Positive Risk Factors

-Age
Male 45 years or older
Female 55 years or older
Family history of premature CHD
– Current cigarette smoker

– Hypertension
BP 140/90 or higher, or on antihypertensive medication
– Low HDL levels: less than 40 mg/dL
-Diabetes mellitus

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Coronary Heart Disease
Negative (Beneficial) Risk Factor

High HDL (“good” cholesterol): 60 mg/dL or higher

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Secondary causes of dyslipidemia

 

  • In patients with type 2 diabetes mellitus (DM), hyperlipidemia occurs in association with insulin resistance and frequently involves increased triglycerides and low serum high density lipoprotein (HDL) cholesterol.

 

  • Excessive alcohol consumption can raise triglyceride levels.

 

 

  • Primary biliary cholangitis and similar disorders may be accompanied by marked hypercholesterolemia that results from an accumulation of lipoprotein-X.

 

  • Marked hyperlipidemia can occur in the nephrotic syndrome due primarily to high serum total and low density lipoprotein (LDL) cholesterol concentrations.

 

  • Dyslipidemia is less prominent in chronic kidney disease (CKD), but CKD is associated with elevations in LDL cholesterol and triglycerides, and low levels of HDL cholesterol; hypertriglyceridemia (type IV hyperlipoproteinemia) occurs in 30 to 50 percent of cases of CKD.

 

  • Hypothyroidism is a common cause of hyperlipidemia, most typically raising LDL cholesterol, but hypertriglyceridemia can also be seen. We suggest screening for hypothyroidism in all patients with dyslipidemia.

 

  • Smoking modestly lowers the serum HDL cholesterol concentrations and HDL atheroprotective properties. (See ‘Cigarette smoking’ above.)

 

 

  • Obesity is associated with a number of deleterious changes in lipid metabolism, including high serum concentrations of total cholesterol, LDL cholesterol, VLDL cholesterol, and triglycerides, and a reduction in serum HDL cholesterol concentration.

 

 

  • A number of medications can affect serum lipid concentrations, either directly or through effects on weight or glucose metabolism: thiazide diuretics, beta blockers, and oral estrogens, atypical antipsychotic agents.

 

Treatment Guidelines

-Antilipemic drugs
Drugs used to lower lipid levels
Used as an adjunct to diet therapy
-Drug choice based on the specific lipid profile of the patient
– All reasonable non-drug means of controlling blood cholesterol levels (e.g., diet, exercise) should be tried for at least 6 months and found to fail before drug therapy is considered

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The different types of antilipemic drugs

-HMG-CoA reductase inhibitors (HMGs, or statins)
-Bile acid sequestrants
-Niacin (nicotinic acid)
-Fibric acid derivatives (fibrates)
-Cholesterol absorption inhibitor (Zetia)
Combination drugs (Vytorin)

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HMG-CoA Reductase Inhibitors (HMGs, or statins)

Most potent LDL reducers

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HMG-CoA Reductase Inhibitors:
Mechanism of Action

-Inhibit HMG-CoA reductase, which is used by the liver to produce cholesterol
-LOWER RATE OF CHOLESTEROL PRODUCTION

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HMG-CoA Reductase Inhibitors:
Indications

-First-line drug therapy for hypercholesterolemia
– Treatment of types IIa and IIb hyperlipidemias
Reduces LDL levels by 30% to 40%
Increases HDL levels by 2% to 15%
Reduces triglycerides by 10% to 30%
– Atorvastatin appears to be more effective in lowering triglyceride levels than other HMG-CoA reductase inhibitors.

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HMG-CoA Reductase Inhibitors:
Adverse Effects & contraindications

Contraindications: allergy, pregnancy, liver disease or elevation in liver enzymes

Adverse Effects:
– Mild, transient GI disturbances, Rash and Headache. ( most common problems)
– Myopathy (muscle pain), possibly leading to the serious condition rhabdomyolysis
– Elevations in liver enzymes or liver disease

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rhabdomyolysis

breakdown of muscle protein accompanied by myoglobinuria
– abnormal urinary excretion of protein can place a severe strain on the kidneys, possibly leading to acute renal failure and even death.

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Atorvastatin (Lipitor)

Pregnancy X

-statin drug
most commonly used drug in this class of cholesterol-lowering drugs.
– to lower total and LDL cholesterol levels as well as levels of triglycerides.
– raise levels of “good” cholesterol, the HDL component
– can be dosed at any time of day. However, bedtime dosing provides peak drug levels in a time frame that correlates better with the natural diurnal (daytime) rhythm of cholesterol production in the body.

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Bile Acid Sequestrants

These drugs are now considered second-line drugs in most cases, less preferred than the more potent statins

– However, they are still a suitable alternative in patients intolerant of the statins.
-Generally these drugs lower the plasma concentrations of LDL cholesterol by 15% to 30%.
– They also increase the HDL cholesterol level by 3% to 8%
– increase hepatic triglyceride and VLDL production, which may result in a 10% to 50% increase in the triglyceride level.

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Bile Acid Sequestrants:
Mechanism of action

– Prevent resorption of bile acids from small intestine
-Bile acids are necessary for the absorption of cholesterol from the small intestine and are also synthesized from cholesterol by the liver. This is one natural way that the liver excretes cholesterol from the body.
-The more that bile acids are excreted in the feces, the more the liver converts cholesterol to bile acids. This reduces the level of cholesterol in the liver and thus in the circulation as well.
-The liver then attempts to compensate for the loss of cholesterol by increasing the number of LDL receptors on its surface. Circulating LDL molecules bind to these receptors to be taken up into the liver, which also has the benefit of reducing circulating LDL in the bloodstream.

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Bile Acid Sequestrants:
Indications

-Type II hyperlipoproteinemia
-Relief of pruritus associated with partial biliary obstruction (cholestyramine)
-May be used along with statins

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Bile Acid Sequestrants:
Adverse Effects & contraindications

contraindications:
drug allergy, biliary or bowel obstruction, and phenylketonuria (PKU)

Adverse effects:
-Constipation
-Heartburn, nausea, belching, bloating
These adverse effects tend to disappear over
time- Increasing fiber and fluid intake may relieve constipation and bloating.

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Cholestyramine (Questran)

Bile Acid Sequestrants drug
-contraindicated in patients with a known hypersensitivity to it and in those who have complete biliary obstruction or PKU.
-It may interfere with distribution of the proper amounts of fat-soluble vitamins to the fetus or nursing infant of a pregnant or nursing woman taking the drug. -Cholestyramine is now being used for its constipating effect, often given as needed for loose bowel movements.

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Niacin (Nicotinic Acid) ) Nicobid

-Vitamin B3
-Lipid-lowering properties require much higher doses than when used as a vitamin
-Effective, inexpensive, often used in combination with other lipid-lowering drugs

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Niacin: Mechanism of Action

-Thought to increase activity of lipase, which breaks down lipids
-Reduces the metabolism or catabolism of cholesterol and triglycerides
– In large doses, it may produce vasodilatation that is limited to the cutaneous vessels. This effect seems to be induced by prostaglandins.
– Niacin also causes the release of histamine, which results in an increase in gastric motility and acid secretion.

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Niacin: Indications

-Effective in lowering triglyceride, total serum cholesterol, and LDL levels
-Increases HDL levels
-Effective in the treatment of types IIa, IIb, III, IV, and V hyperlipidemias

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Niacin: Adverse Effects & contraindications

Contraindications: liver disease, hypertension, peptic ulcer and active hemorrhagic procress

adverse effects:
-Flushing (caused by histamine release)
-Pruritus
-GI distress
– small doses of aspirin or nonsteroidal antiinflammatory drugs (NSAIDs) may be taken 30 minutes before the niacin dose to minimize the cutaneous flushing. These undesirable effects can also be minimized by starting patients on a low initial dosage and increasing it gradually, and by having patients take the drug with meals.

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niacin
drug profile

very effective, inexpensive medication that, as previously mentioned, has beneficial effects on LDL cholesterol, triglyceride, and HDL cholesterol levels.

– Drug therapy with niacin is usually initiated at a small daily dose taken with or after meals to minimize the adverse effects previously discussed.

– Liver dysfunction has been observed in individuals taking sustained-release forms of niacin, but not immediate-release forms. However, newer extended-release dosage forms, which dissolve more slowly than the immediate-release forms but faster than the sustained-release forms, appear to have even better adverse effect profiles, including less hepatotoxicity and flushing of the skin.

– Niacin is contraindicated in patients who have shown a hypersensitivity to it; in those with peptic ulcer, hepatic disease, hemorrhage, or severe hypotension; and in lactating women.
– It is also not recommended for patients with gout.

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Fibric Acid Derivatives (also known as fibrates): Mechanism of Action

-Believed to work by activating lipase, which breaks down cholesterol
-Also suppress the release of free fatty acid from adipose tissue, inhibit synthesis of triglycerides in the liver, and increase secretion of cholesterol in the bile

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Fibric Acid Derivatives: Indications

all decrease the triglyceride level and increase the HDL cholesterol level by as much as 25%.

– Treatment of types III, IV, and V hyperlipidemias

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Fibric Acid Derivatives:
Adverse Effects and contraindications

Contraindications:
– rug allergy and may include severe liver or kidney disease, cirrhosis, and gallbladder disease.

Adverse Effects:
-Abdominal discomfort, diarrhea, nausea
-Blurred vision, headache
-Increased risk of gallstones
-Prolonged prothrombin time
-Liver studies may show increased function

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Gemfibrozil (Lopid)

Fibrate

-decreases the synthesis of apolipoprotein B and lowers the VLDL level. It can also increase the HDL level. In addition, it is highly effective for lowering plasma triglyceride levels.

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Cholesterol Absorption Inhibitor:
EZETIMIBE
 — Ezetimibe is a cholesterol absorption inhibitor that impairs dietary and biliary cholesterol absorption at the brush border of the intestine without affecting the absorption of triglycerides or fat soluble vitamins. Its mechanism appears to involve inhibition of Niemann-Pick C1 like 1 (NPC1L1) protein, which is expressed both in the intestine and the liver, with this inhibition resulting in a net decrease in cholesterol absorption from the intestine

In two randomized, double-blind, placebo-controlled trials, ezetimibe at a dose of 10 mg/day reduced LDL-C by approximately 17 percent. Ezetimibe is also effective as adjunctive therapy to a statin

IMPROVE-IT, the first large trial to directly assess clinical outcomes with ezetimibe plus a statin compared with a statin alone, found that after a median follow-up of six years, patients with an acute coronary syndrome randomized to ezetimibe/simvastatin had a lower rate of the primary composite CV outcome (CV death; MI; hospital admission for unstable angina; coronary revascularization 30 or more days after randomization; or stroke) than those randomized to simvastatin alone (hazard ratio [HR] 0.94, 95% CI 0.89-0.99; seven-year event rates 32.7 versus 34.7 percent)

 

The precise role of ezetimibe relative to other lipid lowering drugs is unclear. Similar reductions in LDL-C can often be achieved simply by maximizing the dose of statins.

 

Ezetimibe may be helpful for avoiding high doses of statins (and potentially increased susceptibility to muscle injury) in patients who do not meet cholesterol goals on low dose statin therapy alone.

Ezetimibe has been well tolerated in clinical trials. When administered alone, the incidence of either myopathy or serum transaminase elevations was similar to that of placebo; when coadministered with a statin, the incidence of serum transaminase elevation has been slightly higher than with statin therapy alone. The manufacturer suggests measurement of liver function tests prior to initiating treatment with ezetimibe plus a statin.

 

Gemfibrozil and fenofibrate have been noted to increase ezetimibe levels although the clinical significance of this is uncertain. Ezetimibe and fenofibrate have been safely used in combination. It is ok use this combination clinically.

 

 

PCSK9 INHIBITORS — Proprotein convertase subtilisin kexin 9 (PCSK9) is a serine protease produced predominantly in the liver that leads to the degradation of hepatocyte LDL receptors and increased low-density lipoprotein cholesterol (LDL-C) levels.

Therapies that lower circulating PCSK9 levels significantly lower LDL-C levels. This category of lipid lowering therapy appears promising in a range of clinical situations.

Monoclonal antibodies that inhibit PCSK9 (PCSK9 abs) reduce LDL-C in a dose-dependent manner, by as much as 70 percent, and by as much as 60 percent in patients on statin therapy. In contrast with many of the other agents that have been used for lipid lowering, these agents also appear to produce substantial clinical benefits; this may reflect the much greater reductions in LDL-C seen with anti-PCSK9 abs than with most other agents.

 

In particular, treatment with PCSK9-abs appears to result in additional reductions in CV risk even in patients already on intensive or maximal statin therapy:

 

 

  • In two open-label trials of the monoclonal antibody evolocumab that were combined for analysis, 4465 patients who had completed one of twelve phase 2 or phase 3 trials of evolocumab were randomly assigned to evolocumab (140 mg injected subcutaneously every two weeks or 420 mg monthly) plus standard therapy, or standard therapy alone The patients in the underlying trials included those on statin therapy (approximately 70 percent), including high-intensity statin therapy (approximately 27 percent), as well as patients who were statin intolerant or who were on no other lipid lowering therapy, and the median duration of follow-up was 11.1 months. Adverse events were similar in both groups (69 versus 64 percent), as were serious adverse events (7.5 percent in each group); neurocognitive events, although uncommon, were more frequent with evolocumab (0.9 versus 0.3 percent). Patients treated with evolocumab had a lower rate of cardiovascular (CV) events (1.0 versus 2.2 percent, hazard ratio [HR] 0.47, 95% CI 0.28-0.78).

 

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Herbal Product: Garlic

-Used as an antispasmodic, antihypertensive, antiplatelet, lipid reducer
-Adverse effects: dermatitis, vomiting, diarrhea, flatulence, antiplatelet activity
-Possible interactions with warfarin, diazepam
-May enhance bleeding when taken with NSAIDs

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Herbal Product: Flax

-Both the seed and oil of the plant are used
-Uses: atherosclerosis, hypercholesterolemia, GI distress, menopausal symptoms
-May cause diarrhea and allergic reactions
-Possible interactions: antidiabetic drugs, anticoagulant drugs

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Herbal Product: Omega-3
Fatty Acids

-Fish oil products
-Used to reduce cholesterol
-May cause rash, belching, allergic reactions
-Potential interactions with anticoagulant drugs

 

 

 

 

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Nursing Implications

-Assess dietary patterns, exercise level, weight, height, VS, tobacco and alcohol use, family history
– Contraindications include biliary obstruction, liver dysfunction, active liver disease
– Obtain baseline liver function studies
-Patients on long-term therapy may need supplemental fat-soluble vitamins (A, D, K)
-Take with meals to decrease GI upset
– Counsel patient concerning diet and nutrition on an ongoing basis
-Instruct patient on proper procedure for taking the medications
-Powder forms must be taken with a liquid, mixed thoroughly but not stirred, and NEVER taken dry
– Other medications should be taken 1 hour before or 4 to 6 hours after meals to avoid interference with absorption
– To minimize adverse effects of niacin, start on low initial dose and gradually increase it, and take with meals
– Small doses of aspirin or NSAIDs may be taken 30 minutes before niacin to minimize cutaneous flushing
– Inform patients that these drugs may take several weeks to show effectiveness

 

Treatment of patients with a history of any of the following is considered “secondary prevention”
Coronary heart disease
Myocardial infarction
Angina
Coronary revascularization
Cerebrovascular disease
Stroke
Transient ischemic attack
Peripheral arterial disease
Multiple risk factors that confer a 10-year risk of CVD >20%
Chronic kidney disease with estimated GFR <45 mL/min per 1.73 m2*

 

 

 

DMD Nephrology Case 2-Nephrotic Syndrome

 

A 40-year-old man has come to your office with the complaint of swelling of his body over the past several months.  He states that approximately 3 months prior to admission he had fallen off his bicycle and bruised his right leg.  He noted swelling in the leg at that time and soon thereafter noted both his legs had become swollen.  Over the past several months he noticed this swelling had increased over his entire body. He reports a 20-lb. weight gain over that period of time.

 

Discussion points:

  • What are the probable causes of total body edema in this patient? (Include a discussion of secondary hyperaldosterone states including: congestive heart failure, cirrhosis, nephrosis, and malnutrition including malabsorption. Additionally, severe hypothyroidism with myxedema or a generalized allergic reaction may give the appearance of body swelling.)
  • Differentiate the between causes of unilateral leg edema and total body swelling.
  • What other historical information will be important in assessing this patient’s problem?

 

He has no history of heart disease and denies PND, DOE, or orthopnea.  He has no history of liver disease and denies a history of jaundice, dark urine or alcohol use.  He does not know of any exposure to any hepatitis and has no history of IV drug use.  He was never told of any problems with his kidney as an adult or a child. His urinary frequency is unchanged over the past two months.

 

Discussion points:

  • Given this patient’s history, is the likelihood of congestive heart failure or cirrhosis likely?
  • What physical exam points should be focused on in this patient with generalized edema? (Signs of heart failure, hepatic dysfunction, hypothyroidism, malnutrition, or nephrotic syndrome including hypertension).

 

On physical exam, he appears grossly edematous and puffy.  His is BP-145/98, P-92, RR-16, and T-98.6F. The patient’s skin shows no signs of jaundice or telangectasias.  He has no signs of palmar errythema.  His face shows swollen eyelids but sclera are not icteric.  Examination of the neck shows no signs of jugular venous distention and no thyromegaly. His lung exams are clear to auscultation and percussion with the exception of decreased breath sounds and dullness to percussion in the bases.  Cardiac exam revealed a non-displaced PMI. Normal S1 and S2 without murmurs, rubs, S3 or S4. Abdominal exams showed the liver to be approximately 9 cm in size. No splenomegaly was appreciated. There were findings of shifting dullness to percussion of the abdomen.  In the periphery the patient had 4+ pitting edema to the level of the sacrum and throughout both legs. The patient had no signs of gynecomastia, testicular atrophy or parotid swelling. The patient’s neurological exam was normal.

 

Discussion points:

  • Given this examination, is it likely that the patient has congestive heart failure as the cause of his generalized edema?
  • Are there signs of cirrhosis present on this examination?
  • What aspect of this examination would suggest this patient has nephrotic syndrome. (Elevated blood pressure, pleural effusions, ascites, and swelling of the eyelids are frequently seen in patients with nephrotic syndrome).
  • What laboratory tests would you order to confirm your diagnosis?

 

A urinalysis revealed 4+ proteinuria with a microscopic exam that revealed several waxy casts, oval fat bodies, no cellular casts, 1 RBC and 1 WBC per high-powered field.  Electrolytes included a BUN of 20 mg/dl, a creatinine of 1.3 mg/dl, other electrolytes, glucose, calcium and phosphorus were normal. A 24-hour urine collection showed 12 grams of protein and a creatinine clearance of 72 ml/min.  LFTs were normal, as was a prothrombin time. The patient’s albumin was 1.9 gr/dl and serum cholesterol was 670 mg/ml. Chest x-rays revealed bilateral pleural effusions without signs of pulmonary venous engorgement or abnormalities in the cardiac silhouette.

Discussion points:

  • Given the above information, what is the diagnosis of this patient?
  • Construct and differential diagnosis of causes of nephrotic syndrome?
  • What diagnostic studies would you send off looking for systemic diseases as a cause of nephrotic syndrome?
  • What would your initial management of this patient be before the results of other tests become available? (Use a salt restricted diet and judicial use of diuretic therapy.)

 

Laboratory tests were sent for antinuclear antibodies, serum complement, and fasting blood sugar which all were normal. A VDRL and Hepatitis B and C serologies were also negative.

 

Discussion point:

  • Would you recommend a kidney biopsy for this patient and why?

 

The patient is informed of his diagnosis of nephrotic syndrome and the potential benefits and risk of a kidney biopsy in looking for the ideology of this problem. He consented and the procedure is done without complications. The results of the biopsy showed evidence of membranous Glomerulonephritis.

 

Discussion points:

  • How common is membranous GN in adult patients with nephrotic syndrome?
  • Can you determine the etiology of the patient’s GN based on the biopsy?
  • What are likely secondary causes of membranous GN in adults? (Include parasitic diseases, viral hepatitis, solid tumors, and certain drugs including gold, penicillamine, NSAIDs.)
  • What is the prognosis for this patient developing end stage renal disease? (Approximately 30% of patients experience complete remission of this disease without therapy. Other patients maintain a stable renal function of 15 years or more while others rapidly progress into chronic renal failure.)
  • Are there predictors regarding which course this patient will take? (Heavy proteinuria for greater than 6 months often portends a poor prognosis.)
  • How would you treat this patient? (Use of corticosteroid and other immunosuppressive agents have been used in improving patients’ initial outcomes.

 

The patient is informed of his prognosis and the diagnosis of membranous GN. He is started on a course of corticosteroid therapy in conjunction with cyclophosphamide. He will be followed up closely for side affects of the medication as well as the effect on the patient’s renal function as well as level or proteinuria.

 

 

DMD Nephrology Case 1 – Acute Renal Failure

 

You are requested to see an 80-year-old man on the surgical service because of an elevated BUN and creatinine. He had just undergone a splenectomy for thrombocytopenia secondary to splenomegaly from underlying chronic lymphocytic leukemia.  Immediately before surgery his BUN was 22 mg/dl, creatinine was 1.3 mg/dl, urinalysis was normal.  When checked two days post operatively, his BUN had increased to 40mg/dl, and creatinine was 3/0 mg/dl.  Urine output for each of the last two days was approximately 250 ml/day.

 

Discussion points:

  • Given the above information, how would you characterize this patient’s kidney problem? (Go through the differential of prerenal, renal and post renal causes of azotemia)
  • What further information do you need to get historically, through the hospital record, and on physical exam on assessing this patient’s problems?

 

The patient denies symptoms of congestive heart failure.  He has not been extremely thirsty over the last several days.  He has had difficulty urinating over the past several years with a weak urinary stream and nocturia 3-4 times per night. His doctor told him that he had BPH but no therapy was given. The patient denies leg pain or flank pain.  The hospital chart is reviewed which showed the patient had significant bleeding in the operative period with several episodes of hypotension with systolic blood pressure in the 80 range.  These episodes lasted for short periods of time less than 5 minutes and returned to normal blood pressure after that period.  His urine output was 700 ml/day immediately after surgery and dropped to 200-300 ml/day over the past two days.  For the three days after surgery his total fluid balance is positive 3 liters.  His only medication postoperatively was analgesia with Dilaudid.  He did receive one dose of Cephalothin preoperatively and none since that time.

 

Discussion point:

  • How does this historical information affect your differential? (Include possibilities of post-obstructive renal failure secondary to prostatism, and acute tubular injury secondary to hypotensive episodes.)

 

The patient’s physical exam showed his T-37 C, RR-14, BP-130/90, P-82 with no orthostatic changes.  His mucous membranes were moist.  Neck pains were 1cm above the sternal angle.  The patient’s lung exam was clear to auscultation and percussion without rales.  Cardiac exam has a normal S1, S2 without S3 or murmurs appreciated.  The patient’s abdomen was soft with slight tenderness over the surgical scar.  No ecchymosis were noted.  The patient had no CVA tenderness or ecchymosis present in the back.  A foley catheter was placed in the patient at that time which showed approximately 50 cc of urine in the patient’s bladder.

 

Discussion points:

  • How does his physical examination help you in determining the cause of this patient’s acute renal failure? (No signs or symptoms of prerenal azotemia, or post renal obstruction. The patient could conceivably have ureteral obstructions or trauma to his ureters during surgery though both seem unlikely?
  • What laboratory tests would you order at this time?

 

A fresh specimen of the patient’s urine is examined under the microscope and showed numerous epithelial cells and brown degenerating cellular casts.  No crystals or WBC’s were noted, and only rare RBC’s were present.  The urine sodium was 40 meq/l.  Urine specific gravity was 1.01.  Repeat BUN and creatinine on the 4th day after surgery are BUN-52 mg/dl, creatinine-3.5mg/dl. Uric acid was 9.2 mg/dl.  A renal ultrasound is done, kidneys are normal in size, and no signs of obstruction are present.

 

Discussion points:

  • What is your diagnosis at this time? (ATN seems most likely secondary to the patient’s episode of hypotension during surgery. Both physical examination and renal ultrasound confirm no signs of bladder obstruction or ureteral obstruction)
  • How would you treat the patient at this time?

 

On day 6 after surgery, the patient’s BUN is 68 mg/dl, creatinine is 4.1 mg/d.  His urinary volumes are between 300-500 ml/day.  Serum electrolytes are NA – 142 mg/dl, K-4.2 mg/dl, Cl-98 mg/dl, HCO3-23 mg/dl.  The patient is started on fluid and salt restriction but he remains oliguric. By day 8 the patient’s BUN is 85 mg/dl, creatinine is 6.3 mg/dl.

 

Discussion points:

  • Is there anything else you would do to manage the patient at this point? (When do you start dialysis on a patient? What are the signs of uremia?)
  • What is the expected course of patients with acute tubular necrosis?

On day 9, postoperatively the patient’s urine output begins to rise to one liter per day, and by day 11 it is up to 3 ½ liters per day.  The patient’s BUN is up to 92 mg/dl, creatinine is 6.9 mg/dl on day 11.

 

Discussion points:

  • Given the patient is now in the polyuric phase of ATN, how would you change his fluid and electrolyte management?

 

On day 12 the patient’s urine output begins to decrease to 1/5 liters per day.  His BUN and creatinine begin to fall.  Fluid and salt restrictions are discontinued.  The patient is discharged from the hospital on day 14 and followed up as an outpatient. His BUN and creatinine returned to normal thre


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