A bedbound 70 kg 40 year old male had no access to water for many days. He is found by a neighbour and brought to the ER. His serum Na is 170 mmol/L.
What is the total water deficit?
Water deficit is calculated by the formula:
Current body water * ((plasma [Na+] / 140) – 1)
Where current body water is about 60% and 50% of lean body weight in younger men and women, respectively, and is 50% and 45% in elderly men and women, respectively.
The water deficit in this case would be:
0.6 * 70 * (170 ÷ 140 – 1), or 9 L.
How would you correct it? For fluid orders, specify the fluid type and rate of administration.
Water should ideally be replaced orally but often this is difficult due to altered sensorium. It is reasonable to provide water intravenously.
One should not allow serum Na to fall by more than 12 meq/L/day.
Since the Na is elevated by 30 mmol/Land that it should not be correct more than 12 meq/L/day, it should be correct over
30 meq ÷ 12 meq/L/day = 2.5 days, or 60 hours.
Therefore, D5W could be administered at
9000 cc ÷ 60 hours = 150 cc/hour.
Recall this does not take into account ongoing losses.
You are called to assess a 45 year old male with diabetes and chronic kidney disease from diabetic nephropathy. He has been admitted to the hospital with a diagnosis of pneumonia. You are told he has:
Serum K = 6.9 mmol/L
HCO3 = 24
Cr = 180 micromol/L
Write your orders for the initial management of this patient’s hyperkalemia. Include doses where indicated.
Typical orders would include:
- Establish IV access.
- Stat ECG
- IV calcium gluconate (if not taking digoxin)
- IV Humulin R 10-20 units X 1 dose
- IV D50W 1 AMP X 1 dose
- Blood sugar with bedside glucometer hourly
- Calcium resonium 30 gram in 50 cc of 70% sorbitol (if nocontraindication)
For a more detailed review on hyperkalemia, try the following links:
Palmer, Biff F. Managing Hyperkalemia Caused by Inhibitors of the Renin-Angiotensin-Aldosterone System. N Engl J Med 2004 351: 585-592
Disorders of Potassium and Acid-Base Balance. American Journal of Kidney Diseases. May 2005 (Vol. 45, Issue 5, Pages 941-949)
A 38 year old woman presents to the ER with 1 week of fevers and malaise. Serum creatinine 1 year ago was 54 micromol/L. 2 days ago when measured in a walk in clinic it was 97 micromol/L. In the ER, her blood pressure is 160/104 mm Hg and serum creatinine is 173 micromol/L. Urinalysis reveals 3+ protein and 3 + blood. Her microscopy shows red blood cells and red blood cell casts.
What would be in your differential diagnosis? What tests would you order at this point?
This patient has acute renal failure. Given the associated hypertension, proteinuria and hematuria, this patient appears to have the nephritic syndrome. The presence of red blood cell casts make us much more confident about the diagnosis of a glomerulonephritis.
We believe this woman has a glomerulonephritis, but the differential diagnosis still remains broad. It would include, but is not limited to, such conditions as:
- Lupus Nephritis
- Post-streptococcal glomerulonephritis
- ANCA (Anti-Neutrophil Cytoplasmic Antibody) -associated vasculitis, such as:
- Wegener’s Granulomatosis
- Microscopic Polyangiitis
- Renal-limited vasculitis
- Anti-Glomerular Basement Membrane (Anti-GBM):
- Antibody disease
- Goodpasture’s disease (if associated with pulmonary hemorrhage)
- IgA Nephritis
- Henoch-Schonlein Purpura
- Endocarditis-associated glomerulonephritis
- Cryoglobulinemic glomerulonephritis
In order to help make a specific diagnosis, a variety of tests can be ordered, though individual nephrologists may not include all of these in the initial workup. These could include:
- Anti-nuclear antibody (ANA)
- C3 and C4 (complements)
- P-ANCA (perinuclear ANCA)
- C-ANCA (cytoplasmic ANCA)
- Anti-GBM (glomerular basement membrane) antibody
- Hepatitis C antibody
Additional testing might also be necessary to look for other manifestations of the underlying disease. For example, in patients with ANCA vasculitis or Goodpasture’s disease, one might find pulmonary hemorrhage – therefore a chest x-ray would be useful.
In the setting of acute renal failure and a rapidly rising creatinine, most nephrologists will also order a CBC +/- a blood film to consider the diagnosis of Hemolytic Uremic Syndrome (HUS) and/or Thrombotic Thrombocytopenia Purpura (TTP). They will generally also order a serum protein immunoelectrophoresis to consider the diagnosis of multiple myeloma with acute cast nephropathy.
In acute renal failure, you would also want to look for potential complications of renal failure and would therefore order:
- Electrolytes (especially K and HCO3)
Given that most of these patients will require a kidney biopsy, one should consider INR and PTT as well as a renal ultrasound.
One patient has a GFR of 5 ml/min and one patient has a GFR of 120 ml/min. Both have a daily urine output of 1.8 L per day.
Please explain how they both can have the same daily urine output despite such large differences in GFR.
Imagine a person with a glomerular filtration rate of 120 ml/min which is equivalent to almost 180 L/day. This means that about 180 litres per day of water (along with solute) is filtered through all the millions of glomeruli in this person’s kidneys. Almost all of this water is reabsorbed along the nephron.
Imagine if this didn’t happen – they would put out about 7.5 L of water in just 1 hour, leading to hemodynamic collapse quite quickly!
Normally, the kidney reabsorbs large amounts of filtered NaCl and water. If a normal person with a GFR of 120 ml/min reabsorbs 99% of all filtered water, the urine output would be:
0.01 * 180 L = 1.8 L per day.
In the patient with 5 ml/min of GFR (advanced chronic kidney disease), this is equivalent to about 7.2 litres per day of water being filtered through all the glomeruli. If only 70% of water is reabsorbed, 30% or:
0.3 * 7.2L = 1.8L will pass as urine.
So, it becomes quite clear that is it possible for urine volume to be preserved even in advanced chronic kidney disease.
In a patient with a GFR of 5 ml/min, can diuretics increase urine output?
In advanced CKD, diuretics can certainly increase urine volume. Since diuretics act along the renal tubules to diminish salt and water reabsorption, if the fraction of reabsorbed water can be decreased, the total urine excretion will increase. This additional water will contain Na and K which can assist in managing the hypertension and hyperkalemia of chronic renal failure.
Do diuretics have any impact on clearance of uremic toxins?
Since diuretics act AFTER filtration has occurred at the glomerulus, they have no impact on clearance of uremic toxins. The total clearance of uremic toxins is determined by the how much water + solute passes through all the glomeruli combined. If we increase urine volume by using diuretics, the same total amount of toxins are excreted, just in a large amount of water.
Do diuretics have any impact on clearance of potassium?
As mentioned above, diuretics can increase urinary potassium excretion. This is not by increasing the amount of K filtered at the glomerulus, but rather by increasing excretion in the distal nephron.
A 67 year old male presents to the ER with a creatinine of 450 m/L. His JVP is low, his mucous membranes are dry and he has postural tachycardia and hypotension. He is felt to be volume depleted and IV normal saline is started. An abdomal ultrasound shows no evidence of hydronephrosis or hydroureter. 3 days later, the patient is clinically euvolemic but the serum creatinine is still 400 m/L.
Has obstruction been truly ruled out? Provide two explanations describing how the patient could be obstructed despite an unremarkable ultrasound on admission.
Obstruction is generally noted on ultrasound due to the accumulation of urine causing the physical distension of the collecting system. If a patient is obstructed but also severe volume contracted, they may not make enough urine to sufficiently distend the collection so that hydronephrosis and/or hydroureter is notable on ultrasound. However, a repeat ultrasound may show hydronephrosis and/or hydroureter after re-expansion of the extra-cellular fluid volume.
Some patients have renal insufficiency due to extrinsic compression of the collecting system, such as in retroperitoneal fibrosis or malignancy. In these cases, one will not see a dilated collecting system on routine ultrasonography.