Case Study: Chronic Renal Failure
History of Present Illness:
Mr. M.A. 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 hrs) and plasmapheresis was conducted (four plasma
exchanges of 1 L each daily for two weeks). After two weeks, the patient’s 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 3 /week.
Patient Case Question 1. Which type of immune hypersensitivity reaction causes the destructive renal
changes in Goodpasture syndrome—type I, II, III, or IV?
Patient Case Question 2. Why were methylprednisolone and azathioprine given to the patient?
Patient Case Question 3. Why was trimethoprim and sulfamethoxazole prescribed with azathioprine
for this patient?
Patient Case Question 4. What is the purpose of plasmapheresis?
During a follow-up visit with a nephrologist in six months, a urinalysis revealed a lowgrade proteinuria
and hematuria.
Patient Case Question 5. What is the pathophysiology behind the clinical signs of proteinuria and
hematuria in this patient?
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 patient’s most recent visit with the
nephrologist, vital signs were: BP 150/95, P 90, RR 22 and unlabored, T 98.6°F, Ht 59, Wt 170 lb. Serum
creatinine test results were compared with previous tests to determine the extent of progression of
renal failure. 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
Patient Case Question 6. Determine the approximate time to end-stage renal disease from this visit.
Patient Case Question 7. Determine the patient’s creatinine clearance from tests done three days ago,
indicate the stage of chronic renal failure to which the patient has progressed, and identify an action
plan.
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.”
Head, Eyes, Ears, Nose, and Throat
Pupils equal at 3 mm, 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
Patient Case Question 8. What is a likely cause of the abnormal lung sounds here?
Heart • Regular rate and 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 • Normal bowel sounds
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
Neurological • Alert and oriented x 3 • No sensory or motor abnormalities • CNs II–XII intact • Muscle
tone 5/5 throughout • Positive Chvostek sign bilaterally
Patient Case Question 9. Describe a positive Chvostek sign and suggest with which abnormal
laboratory test below this clinical sign is consistent.
Na 149 meq/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 32 meq/L ALT 38 IU/L
Proteinurine BUN 143 mg/dL Alk Phos 178 IU/L Bloodurine 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, 8.3 cm each
Hct 30.7% Alb 2.9 g/dL Chest x-ray: bibasilar shadows MCV 80 fL T protein 5.0 g/dL ECG Normal
Patient Case Question 10. There are twenty abnormal laboratory tests above. Identify them and
suggest a brief pathophysiologic mechanism for each.
