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Thursday, March 31, 2011
HyperKalemia Challenge
35yo Indian male with no PMHx presents to PMD for routine physical and labs. He is found to have a K of 6.8meq/l and sent to hospital for admission and w/u. These results are repeated and verified. The patient has no symptoms or any significant PMHx. He denies use of NSAIDs or any other OTC meds or herbs with the exception a pinch of tamaric powder once or twice daily for a couple of weeks due to inadvertent biting of his tongue. He denies high risk behaviour (HIV risk factors).
Exam is unremarkable as are vitals. Serial labs show HCO3 ranging from 20 - 27 (mostly in low to mid 20s). UA is unremarkable with pH running 5.5. Initial UNa 200meq/l and Uk 30 initially, repeated (for TTKG) shows Una 117 and Uk 12 with TTKG <2. His Cr runs from 0.9 to 1.2. His PRA is 0.12 and Aldo <1 at the time of presentation. Serum cortisol is normal. His medicine team orders MRI abd for some reason and adrenals are remarked as "small".
The nephrologist on the case believes he has Type IV RTA, but etiology is unclear to him. He is treated medically and his K ultimately improves and he is discharged home on fludrocortisone.
He is then seen in the office. It was decided to attempt to see if his renin/aldo levels are inducible through volume depletion and also look for aldo synthase deficiency. His fludrocortisone is stopped for 5 days and he is started on Lasix 20mg BID and subsequent labs only on the lasix for 5 days:
Deoxycorticosterone slightly high and 18-Hydroxycorticosterone high, but 11-deoxycortisol, corticosterone, cortisol all WNL and PRA 1.4 and aldo 27! His BP is not typically more than 130s systolic, however the consideration of Gordon's Syndrome (pseudohypoaldo type 2) is given, and the decision try HCTZ and look for response of K and TTKG.
Differential?
Exam is unremarkable as are vitals. Serial labs show HCO3 ranging from 20 - 27 (mostly in low to mid 20s). UA is unremarkable with pH running 5.5. Initial UNa 200meq/l and Uk 30 initially, repeated (for TTKG) shows Una 117 and Uk 12 with TTKG <2. His Cr runs from 0.9 to 1.2. His PRA is 0.12 and Aldo <1 at the time of presentation. Serum cortisol is normal. His medicine team orders MRI abd for some reason and adrenals are remarked as "small".
The nephrologist on the case believes he has Type IV RTA, but etiology is unclear to him. He is treated medically and his K ultimately improves and he is discharged home on fludrocortisone.
He is then seen in the office. It was decided to attempt to see if his renin/aldo levels are inducible through volume depletion and also look for aldo synthase deficiency. His fludrocortisone is stopped for 5 days and he is started on Lasix 20mg BID and subsequent labs only on the lasix for 5 days:
Deoxycorticosterone slightly high and 18-Hydroxycorticosterone high, but 11-deoxycortisol, corticosterone, cortisol all WNL and PRA 1.4 and aldo 27! His BP is not typically more than 130s systolic, however the consideration of Gordon's Syndrome (pseudohypoaldo type 2) is given, and the decision try HCTZ and look for response of K and TTKG.
Differential?
TOPIC DISCUSSION: Residual renal function???
We often associate this term:- residual renal function(RRF) with Peritoneal dialysis and how important that is for fluid management. Why is this not that emphasized in Hemodialysis???
Does residual renal function matter in any dialysis modality? The short answer is yes!!
A recent paper in NDT looked at mortality in 1800 haemodialysis (HD) and peritoneal dialysis (PD) patients in 1996-2006. The investigators estimated a hazard ratio (HR) corresponding to the effect of the full loss of GFR on mortality, as compared to not having fully lost GFR, of 1.50 [95% confidence interval (CI) 1.09-2.07]. The HR corresponding to the effect of GFR when GFR is not (yet) fully lost on mortality was 0.97 (95% CI 0.92-1.02) (per mL/min/1.73m(2)). They found no significant difference in the effect of GFR on mortality between patients starting on PD and HD. They concluded that preventing or delaying the full loss of GFR can improve survival in dialysis patients. This supports the importance that is given to the effect of treatment options for patients with ESRD on the rate of decline of the residual renal function.
Another study found that patients without RRF were older, had lower baseline serum albumin levels and spent 18.6 more days in hospital per year than those with RRF. Mean survival time was significantly lower in patients without RRF (p = 0.027). In a Cox proportional hazards model, only RRF remained as a significant independent predictor.
Another study in CJASN found a strong relation between RRF and improved phosphate and anemia control in HD patients.
Given these recent studies, it appears that RRF is very important in HD patients as well. Perhaps holding ACE-inhibitors and/or angiotensin-receptor blockers, limiting the use of nephrotoxic drugs, avoiding dialysis associated hypotension, avoiding contrast media procedures, adequate control of blood pressure might help preserve that RRF. All three studies are listed below!
Ref:
http://www.ncbi.nlm.nih.gov/pubmed/21242677
http://www.ncbi.nlm.nih.gov/pubmed/21317411
http://www.ncbi.nlm.nih.gov/pubmed/21030579
Does residual renal function matter in any dialysis modality? The short answer is yes!!
A recent paper in NDT looked at mortality in 1800 haemodialysis (HD) and peritoneal dialysis (PD) patients in 1996-2006. The investigators estimated a hazard ratio (HR) corresponding to the effect of the full loss of GFR on mortality, as compared to not having fully lost GFR, of 1.50 [95% confidence interval (CI) 1.09-2.07]. The HR corresponding to the effect of GFR when GFR is not (yet) fully lost on mortality was 0.97 (95% CI 0.92-1.02) (per mL/min/1.73m(2)). They found no significant difference in the effect of GFR on mortality between patients starting on PD and HD. They concluded that preventing or delaying the full loss of GFR can improve survival in dialysis patients. This supports the importance that is given to the effect of treatment options for patients with ESRD on the rate of decline of the residual renal function.
Another study found that patients without RRF were older, had lower baseline serum albumin levels and spent 18.6 more days in hospital per year than those with RRF. Mean survival time was significantly lower in patients without RRF (p = 0.027). In a Cox proportional hazards model, only RRF remained as a significant independent predictor.
Another study in CJASN found a strong relation between RRF and improved phosphate and anemia control in HD patients.
Given these recent studies, it appears that RRF is very important in HD patients as well. Perhaps holding ACE-inhibitors and/or angiotensin-receptor blockers, limiting the use of nephrotoxic drugs, avoiding dialysis associated hypotension, avoiding contrast media procedures, adequate control of blood pressure might help preserve that RRF. All three studies are listed below!
Ref:
http://www.ncbi.nlm.nih.gov/pubmed/21242677
http://www.ncbi.nlm.nih.gov/pubmed/21317411
http://www.ncbi.nlm.nih.gov/pubmed/21030579
Wednesday, March 30, 2011
CONSULT ROUNDS: Ranolazine and the Kidney?
The cardiology world has become used to a new kid on the block in the last 5-6 years called Ranolazine or Ranexa. Ranolazine is indicated for the treatment of chronic angina. It has been shown to decrease angina episodes in individuals with coronary artery disease and it has been shown to both decrease angina episodes and increase exercise tolerance in individuals taking concomitant other anti anginal medications. It doesn't affect the blood pressure or heart rate that much. Ranolazine is believed to have its effects via altering the trans-cellular late sodium current. It is by altering the intracellular sodium level that ranolazine affects the sodium-dependent calcium channels during myocardial ischemia. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia.
Why does this agent matter to us?1. It causes an increase in creatinine? Is it real renal injury or a false elevation? Ranexa produces elevations of serum creatinine by 0.1 mg/dL, regardless of previous renal function. The elevation has a rapid onset, shows no signs of progression during long-term therapy, is reversible after discontinuation of Ranexa, and is not accompanied by changes in BUN. In healthy volunteers, Ranexa 1000 mg twice daily had no effect upon the glomerular filtration rate. The elevated creatinine levels are likely due to a blockage of creatinine's tubular secretion by ranolazine or one of its metabolites.
2. Ranolazine is primarily metabolized by CYP3A and has strong interactions with our transplant drugs calcineurin inhibitors like cyclosporine and tacrolimus. The drug increases the levels of tacrolimus and cyclosporine and could cause renal damage indirectly. Sounds like this is a good agent to use in angina but with caution and possibly in reduction of the CNI doses.
Check out below references:
Tuesday, March 29, 2011
CONSULT ROUNDS: A primer on CVVHDF orders
How does one calculate the prescribed dose on CVVHDF?
Here is an order set:
BFR 150cc/min
DFR 1500cc/hr
Pre pump flow 700cc/hr
Post pump flow 400cc/hr
Ultrafiltration goal 100cc/hr
Our formula for estimated GFR is uv/p ( v=volume, u= urine crt and p= plasma crt). In this case, would be dialysate crt and plasma crt. We have to make one assumption:- since the rate is so slow, the equilibration of dialysate crt and plasma crt would cancel out and your GFR = Volume.
So then, your diffusive clearance would be your DFR, which in this case would be 1500/60 or 25cc/min
your convective clearance would be your pre +post + UF you ordered= 1200/60 or 20cc/min
Hence, you are getting this person 45cc/min of prescribed GFR. Doesn't mean that is the DELIVERED dose.
One more aspect that might be missing is the residual urine output which might be good and might only add to the GFR.
Just an interesting exercise that we should do all time we do CVVHDF orders.
Also, this helps pharmacy guide your medication prescriptions
Monday, March 28, 2011
CLINICAL CASE 33, ANSWERS and SUMMARY
Which one of the following is NOT related to an elevated PTHrp level and leading to hypercalcemia? What you all answered:
SLE 29%
Malignancy 6%
HIV associated Lympadenopathy 8%
Massive mammary hyperplasia during pregnancy 6%
Manganese toxicity 23%
During late pregnancy and lactation in hypoparathyrodism 25%
Close race between SLE, Manganese and Late pregnancy. Correct answer is Manganese toxicity. Rest of all are associated with pthrp production.
All above causes mentioned are rare causes of hypercalcemia to begin with.
Lets get to one by one.
We all know that malignancy such as ovary, lung and kidney can be associated with pthrp associated hypercalcemia. SLE, HIV associated lymphadenopathy has also been associated with pthrp associated hypercalcemia. Apparently, massive mammary hyperplasia during pregnancy, late pregnancy via placenta production of pthrp and lactation in hypoparathyroidism all have been associated with pthrp associated mechanism of hypercalcemia. The hypercalcemia associated with manganese toxicity is due to an unknown mechanism that we don't know( not pthrp).
Below are few causes that I saw in a very interesting article on rare causes of hypercalcemia. Take a look.
Ref is below.
Ref is below.
**Rare causes of hypercalcemia associated with elevated 1,25-dihydroxyvitamin D
1. Wegener’s granulomatosis
2. Cat scratch fever
3. Crohn’s disease
4. Acute granulomatous pneumonia
5. Hepatic granulomatosis in chronic dialysis
6. Talc granulomatosis
7. Silicone granulomatosis
8. BCG therapy
9. 8-Cl-cAMP therapy
10. Lipoid pneumonia
11. Subcutaneous fat necrosis of the newborn
**Rare presentations of the milk-alkali( calcium alkali) syndrome
1. Oyster shell calcium in betel nut chewing
2. Overdose with buffered aspirin
3. Massive cheese ingestion ( tofu perhaps as well)?
4. Munchausen’s syndrome
**Unusual PTHrP-mediated hypercalcemic conditions
1. SLE
2. HIV-associated lymphadenopathy
3. Lymphedema of chest and pleural cavities
4. Massive mammary hyperplasia during pregnancy
5. During late pregnancy and lactation in hypoparathyroidism
6. With benign tumors of ovary and kidney, and in benign pheochromocytoma
** Medications that have been unusually associated with hypercalcemia
1. Omeprazole in acute interstitial nephritis
2. Theophylline toxicity
3. GH in intensive care unit patients
4. Parenteral nutrition
5. Foscarnet
6. Hepatitis B vaccination
7. 8-Cl-cAMP chemotherapy
8. Manganese toxicity
**Rare causes of hypercalcemia in which the mechanism is not known
1. Eosinophilic granuloma
2. Leprosy in rheumatoid arthritis
3. Mycobacterium avium complicating AIDS
4. Cytomegalic virus infection in AIDS
5. Chronic berylliosis
6. Nocardia asteroides pericarditis
7. Diffuse octeoclastosis
8. Paraffin granulomatosis
9. Brucellosis
10. Isolated ACTH deficiency
11. Glucocorticoid withdrawal
12. Hypocaloric diet in hypoparathyroidism
13. Advanced chronic liver disease
14. Type I Gaucher’s disease with acute pneumonia
15. Lymphedema in SLE
16. Juvenile rheumatoid arthritis
17. Lymphadenopathy with high IL-6
**Causes of Pseudohypercalcemia
1. High serum albumin
2. Thrombocythemia
3. Calcium binding to M-proteins
Ref:
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