Disorders of Salt and Water Balance
Acute Renal Failure
Hyperkalemia/hypokalemia
Chronic Renal Failure
Glomerular Disease
Acid-base Disorders

Note:  There are more cases included here than can be discussed in two hours;  therefore, the cases should be used as resources and starting points for discussion;  the cases need not be addressed in order of presentation

Case 1
A newspaper reporter who was in his usual state of good health became lost in the desert of Iraq without food and water for 4 days.  After rescue by a United States Marines expeditionary force patrol, he was sent to the field hospital.  He reported dizziness, weakness, dry mouth, and headache.  Physical exam showed:  temp 98.8, resp 20, BP 100/60 (lying), HR 100 (lying), BP 75/40 (standing), HR135 (standing), a well-developed, sand-covered, unshaven, middle-aged male with dry mucous membranes, clear lungs, no JVD, normal cardiac exam, regular rapid heart rate, no LE edema.  Na 158 mEq/L, K 5.0 mEq/L, BUN 40 mg/dl, S-creat 1.5 mg/dl, urinalysis deep yellow with specific gravity 1.030, otherwise normal.

Case 2
A 60 year-old female has a well-documented history of CHF with an ejection fraction of 25%.  She came to the ER with a 3-day history of shortness of breath, DOE, orthopnea, and PND.  She noted that her weight had increased by 10 pounds over 3 weeks. Medications included lipitor, norvasc, coreg, lisinopril, furosemide.  Physical exam showed:  temp 96.8, resp 28, BP 110/60 (lying), HR 55 (lying), BP 105/60 (standing), HR 58 (standing), an obese female in moderate respiratory distress, rales in the lower half of both lung fields, decreased breath sounds and dullness to percussion over the lower lung fields, JVD, borderline bradycardia with a regular rhythm, S3 gallop, 4+ pitting pretibial edema to the mid thigh.  Na 125 mEq/L, K 5.0 mEq/L, BUN 60 mg/dl, S-creat 1.8 mg/dl, urinalysis normal.

Questions

1. Do these patients have disorders of salt balance?
2. Do these patients have disorders of water balance?
3. How does one distinguish disorders of salt balance from disorders of water balance?
4. Delineate water spaces in the human.
5. Delineate the mechanisms of sodium reabsorption along the nephron.
6. How does the kidney elaborate dilute urine (when needed)?
7. What are the pathophysiological mechanisms that prevent the kidney from elaborating dilute urine, thus allowing hyponatremia to occur?
8. What is the appropriate initial therapy in these patients?

Case
A 75- year old female with a history of recurrent kidney stones complained of progressive left lower quadrant abdominal pain for 6 hours.  EMS was called after her husband found her incoherent and moaning on the floor.  In the ER, she responded to questions by opening her eyes but could not follow commands.  Urine output was 20 cc/hr over the first 3 hours in the ER.  Physical exam showed:  temp 102.8, resp 30, BP 70/40 (lying), HR 70 (lying), an obese female with warm dry skin, clear lungs, no heart murmurs, regular heart rhythm, guarding on abdominal exam and pain on palpation diffusely, worst in left lower quadrant, no LE edema.  WBC 16,000 with 20% band forms, Na 138 mEq/L, K 5.8 mEq/L, BUN 20 mg/dl, S-creat 2.4 mg/dl, urinalysis 30 mg/dl protein, specific gravity 1.010, multiple brown granular casts, 2 RBC/hpf, 1 WBC/hpf.  Labs from 1 month before at a routine primary care visit revealed S-creat of 0.9 mg/dl.

Questions

1. Does this patient have ARF or CRF?
2. What is the differential diagnosis of the cause of RF?
3. What radiological test would be helpful?
4. What other urine studies would be helpful?
5. What does urinary fractional excretion mean?
6. What is the natural history of this disease?
7. What treatment should be instituted?

Case
A 40 year old male presented to the ER with dizziness.  He was a long-term diabetic with retinopathy, below-the-knee amputation, CHF, and chronic kidney disease.  His medications included insulin, lisinopril, valsartan, spironolactone, beta-blocker, calcium channel blocker, furosemide.  Labs showed proteinuria 1.4 g/day, S-creat 2.8 mg/dl, HCO3 21 mEq/L, glucose 550 mg/dl, K 6.9 mEq/L.  Physical exam BP 80/60, HR 35, a few rales at lung bases, bradycardia with regular rhythm, 1+ LE edema.

Questions

1. What is the differential diagnosis of the cause of hyperkalemia?
2. What might the ECG demonstrate?
3. What is the difference between internal and external K balance?
4. How is K handled along the nephron?
5. How should this patient be treated?

Case
The same patient (above) was lost to follow-up after the admission for the treatment of his hyperkalemia.  Five years later, he came to the ER with a month history of fatigue, weight loss, loss of appetite, and nausea in the morning.  Physical exam was normal except for pallor and a tri-partite pericardial rub.   BP 150/90.  Na 135 mEq/L, K 5.6 mEq/L, HCO3 16 mEq/L, calcium 6.7 mg/dl, phosphorus 7.8 mg/dl, BUN 180 mg/dl, S-creat 17.5 mg/dl, Hct 22%, PTH 670 pg/ml.

Questions

1. What is the estimated GFR?
2. What one word describes the constellation of symptoms?
3. What is the cause of the anemia?
4. What is the significance of the cardiac findings?
5. Explain the calcium, phosphorus, and PTH lab findings?
6. How should this patient be treated?

Case 1
A 22 year-old female presented to her gynecologist, who acts as her primary care physician, with weakness, low-grade fever, and arthralgias, and lower extremity edema.  Physical examination revealed temp 100.8, BP 130/70, HR 95, pallor, malar face rash, no JVD, clear lung fields, borderline tachycardia, 4+ pre-tibial edema.  Lab abnormalities included K 5.0 mEq/L, BUN 10 mg/dl, S-creat 0.7 mg/dl, albumin 2.3 g/dl, dipstick urinalysis 300 mg/dl protein, 0-1 WBC/hpf, 0-1 RBC/hpf, quantitation of proteinuria 6.2 g/day.  The patient was started on an angiotensin converting enzyme inhibitor and corticosteroids and did not follow up in renal or rheumatology clinic.

Case 2
The same patient presented again 5 years later with recurrent swelling of the legs and SOB.  Physical examination revealed BP 160/110, HR 95, pallor, face rash, JVD, rales at lower 1/3 of lung fields, dullness to percussion at both lung bases, decreased breath sounds at lung bases, borderline tachycardia, 4+ pre-tibial edema.  Lab abnormalities included K 5.5 mEq/L, BUN 40 mg/dl, S-creat 5.2 mg/dl, albumin 3.5 g/dl, cholesterol 290 mg/dl, dipstick urinalysis revealed 300 mg/dl protein, large blood, and microscopic urinalysis revealed 10 WBC/hpf, 75 RBC/hpf, occasional RBC casts.

Questions

1. What systemic disease does this patient have?
2. What lab tests suggest glomerular disease?
3. What defines the nephrotic syndrome?
4. What is the status of the extracellular fluid volume in each setting?
5. What is the status of the intravascular volume in each setting?
6. What is the difference between acute nephritic syndrome and nephrotic syndrome?
7. Why are nephrotic patients hypercoagulable?
8. What is the most likely renal histology?

Case 1
A 30 year old male diabetic came to the ER with fatigue and vague abdominal pain.  Blood sugar 450 mg/dl, serum ketones positive:

Case 2
A 22 year old female came to the ER with second thoughts after an aspirin overdose.  In fact, salicylates were detected in her blood and urine.

Case 3
A 63 year old male came to the ER with SOB, with a medical history that included alcoholism, CHF.  He was coughing up brownish-green sputum and vomiting in the ER.  Chest x-ray revealed a lobar consolidation.

Questions

1. Is there an acid-base disorder?
2. Are the labs value consistent with each other (Henderson-Hasselbach)?
3. If they were not, why might this be?
4. What is the obvious primary acid-base disorder?
5. Is there another, superimposed acid-base disorder?  ie, how does one investigate for a mixed acid-base disorder?
6. Is there a third acid-base disorder?  ie, how does one investigate for a triple acid-base disorder?
7. Is the acid-base analysis consistent with the clinical scenario?