Case Study-Chronic Renal Failure HISTORY OF PRESENT

Case Study-Chronic Renal Failure HISTORY OF PRESENT ILLNESS Mr. Tyler is a 27-year-old white male, who is visiting his primary healthcare provider to discuss recent blood tests. He has been feeling fatigued and weak lately. PAST MEDICAL HISTORY Three years ago, the patient presented to the emergency room with a six-hour history of coughing up blood. He also complained of difficulty breathing, chills, and chest pain. He had recently suffered a two-week episode of influenza A. Laboratory tests revealed an elevated white blood cell count and iron deficiency anemia. A physical exam revealed moderate hepatosplenomegaly and inspiratory crackles at the base of each lung. He was hospitalized for a thorough clinical workup. An ELISA test was positive for anti-glomerular basement membrane (GBM) antibodies in the blood but serum complement levels were within normal limits. Immunofluorescence of the renal biopsy was positive for IgG and complement lining the glomerular membranes. A diagnosis of Goodpasture syndrome was made. The patient was educated about Goodpasture syndrome (that it is a disease in which the immune system attacks the kidneys and lungs) and that a potential serious complication is chronic renal failure. The patient was immediately placed on methylprednisolone (1 mg/kg/ d po divided Q 6-12 hours) and plasmapheresis was conducted (four plasma exchanges of 1 L each daily for two weeks). After two weeks, the patient symptoms resolved and serum anti-GBM antibodies were no longer detectable. The patient was maintained for six months on azathioprine (2 mg/kg/d po QD) and 160 mg trimethoprim plus 800 mg sulfamethoxazole 3x/week. Patient Case Questions Which type of immune hypersensitivity reaction causes the destructive renal changes in Goodpasture syndrome-Type I, II, III or IV? Why were methylprednisolone and azathioprine given to the patient? What is the purpose of plasmapheresis? During a follow-up visit with a nephrologist in six months, a urinalysis revealed a low-grade proteinuria and hematuria. 4. What is the pathophysiology behind the clinical signs of proteinuria and hematuria in this patient? Clinical Course With each patient visit at every six-month interval, proteinuria and hematuria became more severe. Also, increasing BUN and serum creatinine levels indicated that kidney disease was progressing. The patient had one relapse at one year following onset and had been hospitalized and treated again with methylprednisolone, azathioprine, and plasmapheresis. At the patients, most recent visit with the nephrologist, vital signs were: BP 150/95, P 90, RR22 and unlabored, T 98.6F, Ht. 5’9″, Wt. 170 lbs. Serum creatinine test results were compared with previous tests to determine the extent of progression of renal failure. Serum Creatinine Measurement Serum Creatinine Concentration (mg/dL) At onset of disease 3 years ago 1.00 6 months after onset 1.18 1 year after onset 1.39 18 months after onset 1.72 24 months after onset 2.38 30 months after onset 3.57 3 days ago, 7.14 Review of Systems The patient denies any bleeding and bruising, shortness of breath, chest pain with inspiration, anorexia, nausea, vomiting, loss of coordination, unsteady gait, and bone pain. He states, however, that his “skin has been itching some lately. I have been using a lot of lotion on my arms and legs, because sometimes it is really bothersome.” Physical Examination and Laboratory Tests The patient is very pale and appears to be in mild acute distress. There is some periorbital edema and mild swelling of his hands. He reports a dull headache for the past four days. “I have been forgetting things a lot lately and I can’t seem to concentrate at work anymore.” HEENT Pupils equal at 3mm, round, and reactive to light and accommodation Extra-ocular muscles intact Anti-icteric sclera Fundi normal Conjunctiva normal Tympanic membranes intact and clear No exudates or erythema in oropharynx Skin Very pale, dry with flakiness No ecchymoses or purpura Neck Supple without masses or bruits Thyroid normal No lymphadenopathy Lungs Mild bibasilar crackles with auscultation 5. What is a likely cause of abnormal lung sounds here? Heart Regular rate rhythm S1 and S2 sounds clear with no additional heart sounds No murmurs or rubs Abdomen Soft, non-tender, and non-distended No guarding or rebound with palpation No masses, bruits, hepatomegaly, or splenomegaly Rectal/Genitourinary Prostate normal in size with no nodules Anal sphincter tone normal Stool is guaiac-negative Extremities Negative for cyanosis or clubbing Mild (1+) edema of the hands and feet Normal range of motion throughout 2 + dorsalis pedis and posterior tibial pulses bilaterally Neurologic Alert and oriented x 3 No sensory or motor abnormalities CNs II-XII intact DTRs=2 + throughout Muscle tone 5/5 throughout Positive Chvostek sign bilaterally 6. Describe a positive Chvostek sign and suggest with which abnormal laboratory test below this clinical sign is consistent. Laboratory Blood Test Results Na 149meq/L Plt 270,000/mm3 Mg 3.8 mg/dL K 5.4 meq/L RBC 3.4 million/mm3 PO4 5.9 mg/dL Cl 116 meq/L WBC 9,400/mm3 PT 14.2 sec Ca 6.7 mg/dL AST 18 IU/L PTT 34 sec HCO3 32meq/dL ALT 38 IU/L Protein urine + + + BUN 143 mg/dL Alk Phos 178 IU/L Blood urine + + + Cr 7.1 mg/dL Glu, Random 152 mg/dL pH Blood 7.45 Hb 9.5 g/dL T bilirubin 2.0 mg/dL Renal Ultrasound: significant bilateral atrophy, 8.3cm each Hct 30.7% Alb 2.9 g/dL Chest x-ray: bibasilar shadows MCV 80fL T protein 5.0 g/dL ECG Normal 7. There are twenty abnormal laboratory tests above. Identify them and suggest a brief pathophysiologic mechanism for each.

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