GU/Patient Problem Solving Seminar 3: Renal Failure & Sodium Disorders

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Case 1

A 70 year old male presents with anorexia, chronic malaise, and has 3+ proteinuria, and occasional red cells on urinalysis. The patient's urea is 35 mmol/L (2.5-7.0), creatinine 700 μmol/L (55-120), hemoglobin 90 g/L (135-180), sodium 135 mmol/L (133-148), potassium 7.5 mmol/L (3.5-5.5), chloride 103 mmol/L (95-105) and CO2 19 mmol/L (24-31), calcium 1.8 mmol/l (2.2-2.6), phosphate 2.2 mmol/l (0.8-1.4), albumin 30 g/l (40-45) and alk phos 150 (50-100).

Urea:Creatine ratio = 35 000 / 700 = 350 / 7 = 50 (very high)

  1. Which lab abnormality in this patient requires the most urgent correction?
    • Hyperkalemia
  2. List 2 treatments which would transiently correct this abnormality: What other options should be considered?
    • Glucose, then insulin; Carbonate; Calcium to stabilize the heart membrane
    • Increased aldosterone would also affect the potassium intracellularly (by the RAAS)
    • Beta agonists would also lower the surum calcium (e.g., ventolin)
    • Alkalosis will also shift the potassium intracellularly
    • Dialysis may also work
    • Principle: Affect in, out or shift
  3. What other associated problems does this patient suffer from and how might they be managed?
    • The patient appears to have anemia (lack of erythropoietin), high Creatine, low calcium (due to high phosphate; low activated vitamin d), high phosphate (inability to clear phosphate)
  4. Is there a case for protein restriction to slow progression of renal disease here?
    • Protein restriction should be avoided because he's already low on protein and is probably averse to eating it.

Case 2

A 24 year old male has undergone splenectomy following a motor vehicle accident to control hemorrhage and shock. The patient has received several blood transfusions pre- and intra-operatively and his blood pressure has been sustained, although it had dropped as low as 80/30 for 2 to 3 hours pre-operatively. The patient returns from the O.R. and you are contacted because he is putting out less than 30 cc's urine/hour although his BP is 140/90.

  1. What kidney condition has this patient likely developed?
    • Acute tubular necrosis
  2. What features of the patient's history could contribute to his current problem?
    • The low blood pressure is the most likely reason
  3. What issues should you focus on with your physical exam?
    • Ruling out muscle crushing (?)
  4. What laboratory tests might aid in the diagnosis of this patient?
    • Creatinine would be helpful
    • Urinalysis
  5. How would you manage the case?
    • Supportive therapy until it is clear that there is an acute condition
    • A little bit of urine

Case 3

A 75-year-old man comes to see you in follow-up for osteoarthritis, which has recently become worse requiring treatment with an NSAID. He also has long-standing hypertension for which he is on Dyazide (triamterene & hydrochlorothiazide), enalapril (an ACE Inhibitor), and atenolol (β blocker). You decided to do biochemistry:

 Urea:                 20 mmol/L
 Creatinine:           200 μmol/L
 Na, Cl, bicarbonate:  normal
 K:                    6.2 mmol/L
 Urinalysis:           1+ protein

Urea:Creatine = 20 000 / 200 = 200 / 2 = 100

You then order a renal ultrasound which shows some reduction in the size of both kidneys. You note that 3 months ago, urea and creatinine were 10 mmol/L and 140 μmol/L respectively.

U:C = 10 000 / 140 = 1 00 / 1.4 = 70

  1. What is the most likely underlying cause of the small kidneys and chronic renal impairment?
    • Hypertension is associated with small kidneys (#2 cause of kidney disease)
  2. What other possibilities might you consider?
  3. What is the cause of the recent deterioration?
    • The NSAIDs blocked the prostaglandins which would have dialated his afferent arterioles. This then caused the GFR to drop
  4. What is the management?
    • Take him off of the drugs
  5. Why is the potassium elevated?
    • The potassium is elevated because he is on a β blocker, ACE inhibitor, and potassium-sparing diuretic, all of which promote hyperkalemia.

Case 4

A 30-year-old woman is seen in the Emergency because of general malaise, nausea and vomiting. Three weeks prior to this she completed a two week course of trimethoprim-sulpha (Septra) for the treatment of pyelonephritis. The urinalysis shows 1+ protein, 20-30 WBC/hpf and 5-8 RBC. There are no casts. The serum creatinine is 900 μmol/L (up from 80 12 months previously) and the urea is 30 mmol/L.

30 000 / 900 = 300 / 9 = 33

  1. Describe your diagnostic approach.
    • This woman has acute renal failure
    • Ascertain whether it is pre-, intra- or post- renal.
  2. What is the most likely diagnosis?
    • This is likely an acute interstitial nephritis, caused by the septra
  3. How can this diagnosis be confirmed?
    • Biopsy, though this is not likely required immediately
  4. What is the treatment?
    • Stop the antibiotics that she is on, and perhaps give a short course of steroids, which would likely avoid the possibilities of deterioration

Case 5

A 70 year old male presents with a history of progressive anorexia, weight loss and itch. On exam there was fluid overload and evidence of malnutrition. Urine sediment was bland, blood urea was 35 mmol/L and serum creatinine 1150 μmol/L, K 5.8, HCO3 17. Ultrasound showed bilateral hydronephrosis and an empty bladder.

  1. What are likely causes of this presentation?
    • The likely cause is some postrenal obstruction that happens before the bladder
  2. How would you manage this case?
    • nephrostomy tube
  3. What complications might arise during treatment?
    • post obstruction diuresis: this arises because of the dump that will happen of urea; this will cause a large obligate water loss to get rid of the urea osmoles

Case 6

A 55 year old woman presents with generalised edema. On exam, there are pleural effusions, ascities, leg edema ++, sacral edema++, and a normal JVP. Urinalysis shows proteinuria +3, serum creatinine is 120 μmol/l and albumin is 28 g/l. She has been treated with Furosemide 80 mgs daily but the edema has not responded.

  1. What is the differential diagnosis of generalized edema?
    • Cirrhosis; CHF; generally an inability to clear salt (not an issue of albumin); renal failure; nephrotic syndrome
  2. What is the mechanism of edema formation here?
    • The interstitial volume must gain a couple of litres to cause edema
    • This is an issue of holding onto salt
  3. How would you achieve an effective diuresis?
    • Restrict salt intake; increase salt output; encourage shift
  4. What side effects of your suggested treatment need to be considered?
    • Can be ototoxic
    • Can cause hypo or hyperkalemia
    • HCT increases absorption of calcium

Case 7

A 60 year old woman presents with abdominal pain, distension and vomiting. Blood pressure is 70/40. A diagnosis of partial small bowel obstruction secondary to adhesions is made by the surgical team and they suggest a conservative approach with no intake by mouth, a nasogastric tube and i/v fluids. Blood urea is 20 mmol/l (3-6 mmol/l) and creatinine is 120 μmol/l (50-110 μmol/l). Sodium is 130 mol/l, potassium 3.3 and bicarbonate 28 mmol/l.

  1. Comment on the patient's volume status.
    • The patient is volume depleted: vomit; low bp, etc.
  2. Comment on the urea creatinine ratio.
    • 20 000 / 120 = 200 / 1.2 = 100 / .6 = 166.7
    • When dry, the body tries to hold on to as many osmoles as possible.
  3. What i/v fluid regimen would you prescribe immediately?
    • saline with potassium until his blood pressure rises and he turns off the aldosterone
  4. What would you prescribe the following day, presuming the patient has stabilized but is still partially obstructed?
  5. If the patient received one liter i/v of 0.45 saline in 5% dextrose, what proportions of that liter would distribute in the ECF and ICF respectively?
    • Split into water and saline:
    • Water: 166mL into ECF; 333 into ICF
    • Saline: ALL (500mL) into ECF
    • Total: 666 ECF: 333 ICF

Case 8

A 75-year-old male who lives alone was found unconscious at home. On exam, there was a dense left hemiplegia consistent with a recent 'stroke', blood pressure was 90/60. Serum sodium was 160 mmol/l, urine sodium was 6 mmol/l.

  1. How would you diagnose this patient's total body Na content and do you think it is high, low or normal?
    • Serum sodium is high, especially because it seems that he is also deficient in volume
  2. What features of this patient’s condition caused him to develop hypernatremia?
    • He lost mucho water, and is now trying to retain salt so he can be thirsty and drink
  3. Why do some volume depleted patients develop hyponatremia and others hypernatremia?
    • Those who can appropriately respond to the thirst mechanism may end up with hyponatremia, and those without the ability to respond end up with hypernatremia

Case 9

A 70 kg. man has severe congestive heart failure. His JVP is elevated and he has pitting edema to the knees. He has no past history of renal disease and he is non-diabetic.

Lab:    Na          130 mmol/L
        Cl          103 mmol/L
        K           4.5 mmol/L
        Creatinine  130 mmol/L
        Urea         12 mmol/L
        Glucose       5 mmol/L
  1. Calculate the patient's serum osmolality.
    • 2Na+ + Urea + Glucose = 277
  2. Is the serum hypotonic, isotonic or hypertonic?
    • Hypotonic hyponatremia
  3. How would you determine his total body Na content?
    • Clinical exam (JVP). His total body sodium is increased, as shown with the JVP
  4. Is his total body Na content increased, decreased or normal?
  5. In this patient, what is the mechanism underlying his hyponatremia and how might you correct it?
    • Decreased effective volume is likely causing an ongoing ADH effect
    • Fix the heart pump; put him on an ACE inhibitor