GU/Patient Problem Solving Seminar 3: Renal Failure & Sodium Disorders
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)
- Which lab abnormality in this patient requires the most urgent correction?
- 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
- 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)
- 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.
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.
- What kidney condition has this patient likely developed?
- Acute tubular necrosis
- What features of the patient's history could contribute to his current problem?
- The low blood pressure is the most likely reason
- What issues should you focus on with your physical exam?
- Ruling out muscle crushing (?)
- What laboratory tests might aid in the diagnosis of this patient?
- Creatinine would be helpful
- How would you manage the case?
- Supportive therapy until it is clear that there is an acute condition
- A little bit of urine
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
- 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)
- What other possibilities might you consider?
- 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
- What is the management?
- Take him off of the drugs
- 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.
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
- Describe your diagnostic approach.
- This woman has acute renal failure
- Ascertain whether it is pre-, intra- or post- renal.
- What is the most likely diagnosis?
- This is likely an acute interstitial nephritis, caused by the septra
- How can this diagnosis be confirmed?
- Biopsy, though this is not likely required immediately
- 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
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.
- What are likely causes of this presentation?
- The likely cause is some postrenal obstruction that happens before the bladder
- How would you manage this case?
- nephrostomy tube
- 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
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.
- 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
- 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
- How would you achieve an effective diuresis?
- Restrict salt intake; increase salt output; encourage shift
- What side effects of your suggested treatment need to be considered?
- Can be ototoxic
- Can cause hypo or hyperkalemia
- HCT increases absorption of calcium
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.
- Comment on the patient's volume status.
- The patient is volume depleted: vomit; low bp, etc.
- 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.
- What i/v fluid regimen would you prescribe immediately?
- saline with potassium until his blood pressure rises and he turns off the aldosterone
- What would you prescribe the following day, presuming the patient has stabilized but is still partially obstructed?
- 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
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.
- 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
- What features of this patientÃ¢â‚¬â„¢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
- 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
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
- Calculate the patient's serum osmolality.
- 2Na+ + Urea + Glucose = 277
- Is the serum hypotonic, isotonic or hypertonic?
- Hypotonic hyponatremia
- How would you determine his total body Na content?
- Clinical exam (JVP). His total body sodium is increased, as shown with the JVP
- Is his total body Na content increased, decreased or normal?
- 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