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INTRODUCTION

Hyperparathyroidism (HPT) is a rather frequent disease, but not fully understood.

Although most part of the cases is presented in clearly defined clinical pictures, some patients

present atypical features.

Surgical treatment is of great value for primary, secondary and tertiary HPT.

Postoperative course is also variable and it is not completely predictable. Right after the

operation, most attention is directed to hypocalcemia, avoiding severe calcium level drop.

Hypocalcemia may be caused by postoperative hypoparathyroidism, but it may be also related to

bone remineralization. Even experienced authors did not mention renal function modification in

this period and they refer that many patients are discharged on a same day or on a next day basis

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.Some years ago, one of the authors (LEI) observed a slight increase of creatinine levels in

some renal transplant patients submitted to parathyroidectomy. In one publication, preoperative

creatinine ranged from 0.9 to 1.7 mg/dL (mean 1.15 mg/dL), while postoperative levels ranged

from 1.0 to 3.1mg/dL (mean 1.27 mg/dL).2

Besides this observation, other authors reported the

loss of residual diuresis in dialytic patients after parathyroidetomy3.

Dr. Maria Odete Ribeiro Leite, an endocrinologist, made comments on a slight edema

after parathyroidectomy for primary HPT, usually resolving in few days (personal

communication). Although uncommon, a clinically significant decrease of renal function after

parathyroidectomy has been observed in some patients with primary HPT. In those cases, blood

pressure fluctuations during anesthesia were suspected as the cause, but not conclusively, because

no report of these fluctuations could be detected in anesthesia records.

Recently, Schwarz et. al. showed a decreased renal function in kidney transplant patients

after parathyroidectomy4. Creatinine levels increase after parathyroidectomy in transplanted

patients was previously mentioned by others5,6. In primary HPT, decreased renal function was a

collateral observation in a study 20 years ago7. In another study, a non significant elevation of

creatinine, a significant increase of u rea, a significant reduction in creatinine clearance in patients

undergoing parathyroidectomy for primary HPT, but without change in glomerular filtration rate

analyzed by the clearance of51

Cr-EDTA8.

These accounts led to some questions regarding the frequency of renal changes in patients

submitted to parathyroidectomy in tertiary HPT. Would this change occur in kidney transplant

patients undergoing other operations in the head and neck? If related to parathyroidectomy, what

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would be the role of HPT? If related to HPT, what might be expected in patients with primary

HPT?

The aim of this study was to evaluate the possible fluctuation of renal function after

parathyroidectomy. By a retrospective analysis, the frequency of renal changes were compare din

different surgical treatment groups, as follows: primary HPT, tertiary HPT after renal

transplantation, non parathyroid related head and neck tumors in kidney transplant patients and

patients with normal renal function and non parathyroid related head and neck tumors (oral,

larynx, pharynx, thyroid, salivary glands cancer or goiter).

PATIENTS AND METHODRetrospective evaluation of primary HPT of different causes and HPT after successful

kidney transplantation (tertiary HPT) submitted to parathyroidectomy at the Department of Head

and Neck Surgery of the University of So Paulo Medical School, from 1997 to April, 2007.

Kidney transplant patients without HPT submitted to resection of other head and neck

tumors under general anesthesia (OKDTx) was analyzed as a control group to patients with

tertiary HPT.

A random sample of patients with normal renal function undergoing surgical treatment for

goiter, thyroid cancer or other head and neck tumors (OHN) was considered as a control group

for primary HPT patients.

Available data of preoperative creatinine and postoperative results were investigated at

the patients charts, from the surgical notes of the first author or available at the electronic system

from the laboratory database from the institution.

The most recent available preoperative creatinine result was considered in relation to

highest postoperative level observed. A subtraction of the preoperative level from the

postoperative was calculated and then, this difference was divided by the preoperative level. The

percentual variation was estimated. This probably reflects changes in renal function. A negative

result was due to a decrease in creatinine reflecting an improvement in renal function. On the

other hand, a positive result indicated an elevation of creatinine and, consequently, a decreased

renal function.

After parathyroidectomy, the change in renal function was considered if superior to 10%.

This restriction tried to avoid variations related to measurement of creatinine, according to the



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variation coefficient from previous studies, about 4%9. The change was stratified to estimate the

magnitude of variation. If a 30% increase from preoperative level was observed, this was

considered a significant change. 6

During the period of study, laboratory employed different methods. Early measurements

were reported as serum automatized colorimetric (normal range 0.6 to 1.4 mg/dl). Later, an

automatized kinetic was employed (normal ranges 0.4 to 0.9 for women and 0.7 to 1.2 form

men). Each patient comparison was done only with the same method.

STATISTICAL ANALYSIS

Descriptive statistics included mean, median, standard deviation (SD), and standard errorof the mean (SEM).

For statistical inference, parametric or non-parametric tests were employed according to

the normality test. A dichotomy of values of less or equal to 10%, or superior to 10% was

checked with the Qui-square test.

Kruskal-Wallis, Dunns Multiple comparison, Mann-Whitney and non-paired student

were employed. Calculated descriptive value (p) was considered significant if inferior to 5%.

RESULTS

In the established 10 year period, 168 primary HPT cases were operated at the institution.

Standard surgical technique was bilateral parathyroid exploration. In 105, creatinine levels could

be compared right after the operation. They were studied as primary HPT group. Data from 38

kidney transplant patients with HPT submitted to surgery were available, and also from seven

transplanted patients without HPT operated on head and neck tumors.

In 25 patients undergoing thyroidectomy, comparative creatinine was available. Of these,

three were submitted to thyroid lobectomy only and one patient with a previous thyroidectomy in

the past underwent a central neck dissection. Total thyroidectomy or completion thyroidectomy

was the operation of the remaining 21 patients. Of these, seven were associated with central neck

dissection.

Table 1 shows the count of cases with creatinine increase superior to 10%, according to

each group.



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Table1 Counts ofcreatinine increase superior to 10%, according to different groups.

CreatinineIncrease Primary HPT Tertiary HPT OK DTx L obectomy Total Thyroidectomy OHN

Negativeor 10% 77 32 1 0 11 3

Total 105 38 7 3 22 18

Comparison of the groups of Table 1 by qui-square test yielded p50% 18

(17.1%)

9

(23.7%)

0

(0%)

3

(13.6%)

0

(0%)



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Table 3 shows descriptive statistics observed in different groups.

Table3 Creatinine variation in different groups.

Tertiary HPT OK DTx Primary HPT Total thyroidectomy OHN

minimum -33.3% -28.0% -20.2% -29.6% -33.3%

maximum +172.5% +38.0% +304.5% +88.9% +43.4%

mean +39.5% -2.7% +30.8% +18.7% -6.4%

median +28.3% -6.0% +25.0% +11.25% -7.5%

SEM 6.4% 8.4% 4.1% 6.8% 4.1%SD 39.2% 22.2% 41.8% 31.7% 17.5%

Normality test passed passed failed passed passed

According to creatinine increase, multiple group comparison did show a significant

difference (p


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Graphic 3 Distribution of postoperative creatinine change in primary HPT (HPT primrio) and OHN (CEC CCP).

These observations suggested two other comparisons. The first one between patients

undergoing parathyroidectomy for primary HPT and those submitted to total thyroidectomy with

or without central neck dissection, but a demonstrated reduction of postoperative parathyroid

hormone level. No statistical difference was observed (p=0.97, Mann-Whitney test), as shown isgraphic 4.



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Graphic 4 Postoperative change of creatinine (% variao da creatinina no PO) in patients with

primary HPT (HPT p rimrio) and total thyroidectomy with hypocalcemia (hipocalcemia PO).

The second comparison tried to answer if a difference between those with presumed

hypoparathyroidism after thyroidectomy could exist when they were compared to those without

postoperative reduction in parathyroid activity. In this condition, patients submitted to thyroid

lobectomy were included in the group of those without postoperative hypoparathyroidism. When

thyroidectomy patients were stratified according to presumed hypoparathyroidism a significant

difference was noted. Mean percent creatinine increase was + 28.5% (SEM 9%) in those with

presumed hypoparathyroid and it was + 1.2% (SEM 5%) in those without evidence of

postoperative hypoparathyroidism. (p=0.02, non paired t test, Graphic 5).



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Graphic 5 Comparison after thyroidectomy with presumed hypoparathyroidism (hipocalcemia) and

without evidence of postoperative parathyroid dysfunction (sem hipocalcemia).

In most cases, creatinine levels return to basal in few days. Graphic 6 illustrates one

patient submitted to total thyroidectomy. She has received supplemental calcium after the

thyroidectomy and the medical team in charge had sampled calcium, parathyroid hormone andcreatinine in the postoperative period. This case also illustrates that creatinine variation is not

associated with serum calcium values, as many patients have received supplemental calcium.



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C r eat in i n e v ar iati on aft er t h y r oi d ect omy i n on e cas e

0,76

1,06

0,73

0,69

0,91(estimated

value)

0

0,2

0,4

0,6

0,8

1

1,2

p r e o p e r ative o p e r atio n 1P O 3P O 9P O

T im e

Creatinine

(mg/dl)P T H


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Through a clinical observation, the present study seems to demonstrate a parathyroid

hormone hemodynamic effect on the kidney as suggested by some previous animal studies where

a decline in glomerular filtration was observed after parathyroidecotmy10,11. These animals did

not have preoperative elevated levels of parathyroid hormone as some thyroid patients of the

present study.

A creatinine change as consequence of blood pressure changes in anesthesia seems not

probable to explain all cases, as patients with head and neck neoplasms undergo more extensive

operations, with more pronounced fluid loss, and in many of them creatinine levels decreased.

Evaluation of renal function by creatinine measurement is questionable, but it is still a

reality in clinical practice

12

. The possible interference of drugs, as cephalosporins or increase inbilirubin13, is apparently less probable in these cases. There is an observation that creatinine

clearance is overestimated in some patients with HPT8, suggesting that the creatinine increase is

not a real change in renal function. However, how can one explain creatinine increase in some

thyroidectomy patients, without previous HPT?

The retrospective nature of this study is associated with many doubts and caution in

interpretation of these observations is advised. Clearly, a prospective study, with other markers of

renal function, as cystatin C, would be of interest. Even measurement of bilirubin would be

justified, as parathyroid hormone affected hepatic flow in an experimental study14

.

There is evidence that renal disease is a world problem of public health, affecting 5% to

10% of population, with progressive loss of kidney function, cardiovascular disease and early

death15. The knowledge of nephrotoxic drugs (anti-inflammatory, antibiotics and radiological

contrasts) make their use selective, with protective measures, lowering their risk of renal

complications.

Recognizing that the surgical treatment of the parathyroid glands by itself may interfere

with renal function is of clinical value. Patient counseling before the operation and careful

preoperative evaluation of renal function are necessary.

Postoperative care is also recommended as the present authors observed a few patients

with a permanent or a progressive loss of renal function after the parathyroidectomy. Indeed,

Edvall showed renal alterations due to HPT16

. Some are functional and revert after excision of

hyperactive parathyroid tissue. However, in some cases, HPT seems to promote an organic



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tubular lesion that is irreversible. In advanced disease, parathyroidectomy may represent the loss

of compensatory mechanism16

.

Special attention should be directed to patients with single kidney, to those with a

previous compromise in renal function, and to those at risk groups, as diabetics and hypertensive

patients.

REFERENCES

1. Wells Jr SA, Doherty GM. The surgical management of hyperparathyroidism. In: Bilezikian JP, Marcus R, Levine

MA, eds. The Parathyroids. 2nd ed. San Diego: Academic Press; 2001. p.487-97.

2. Ianhez LE. Transplante Renal. Seguimento a longo prazo. So Paulo: Lemos Editorial; 2002. p.37.

3. Tzanakis I, Alifieris E, Kagia S, Spantidakis V, Girousis N, Galis A, Kallivretakis N. Does parathyroidectomy

affect residual diuresis in hemodialysis patients? Nephron. 2000;86(3):402-3.

4. Schwarz A, Rustien G, Merkel S, Radermacher J, Haller H. Decreased renal transplant function after

parathyroidectomy. Nephrol Dial Transplant. 2007;22(2):584-91.

5. Evenepoel P, Claes K, Kuypers D, Maes B, Vanrenterghem Y. Impact of parathyroidectomy on renal graft

function, blood pressure and serum lipids in kidney transplant recipients: a single centre study. Nephrol Dial

Transplant. 2005;20(8):1714-20.

6. Rostaing L, Moreau-Gaudry X, Baron E, Cisterne JM, Bernadet-Monrozies P, Durand D. Changes in blood

pressure and renal function after subtotal parathyroidectomy in renal transplant patients presenting persistent

hypercalcemic hyperparathyroidism. Transplant Proc. 1997;29(1-2):204-6.

7. Jones DB, Jones JH, Lloyd HJ, Lucas PA, Wilkins WE, Walker DA. Changes in blood pressure and renal function

after parathyroidectomy in primary hyperparathyroidism. Postgrad Med J. 1983;59(692):350-3.

8. Salahudeen AK, Thomas TH, Sellars L, Tapster S, Keavey P, Farndon JR, Johnston ID, Wilkinson R.

Hypertension and renal dysfunction in primary hyperparathyroidism: effect of parathyroidectomy. Clin Sci (Lond).

1989;76(3):289-96.

9. Myers GL, Miller WG, Coresh J, Fleming J, Greenberg N, Greene T, Hostetter T, Levey AS, Panteghini M, Welch

M, Eckfeldt JH; National Kidney Disease Education Program Laboratory Working Group. Recommendations for

improving creatinine serum measurement: a report from the Laboratory Working Group of the National Kidney

Education Program. Clin Chem. 2006;52(1):5-18.

10. Zaladek-Gil F, Costa-Silva VL, Malnic G. Effects of parathyroid hormone on urinary acidification in the rat.

Braz J Med Biol Res. 1991;24(10):1063-6.

11. Zaladek Gil F, Nascimento Gomes G, Cavanal MF, Cesar KR, Magaldi AJ. Influence of parathyroidectomy and

calcium on rat renal function. Nephron. 1999;83(1):59-65.

12. Pecoits-Filho R. Diagnstico de doena renal crnica: avaliao da funo renal. J Bras Nefrol.

2004;26(Supl.1):4-5.



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13. Weber JA, van Zanten AP. Interferences in current methods for measurements of creatinine. Clin Chem.

1991;37(5):695-700.

14. Charbon GA, Hulstaert PF. Augmentation of arterial hepatic and renal flow by extracted and syntheticparathyroid hormone. Endocrinology. 1974;96(2):621-6.

15. Moe SM, Dreke T, Lameire N, Eknoyan G. Chronic kidney disease-mineral-bone disorder: a new paradigm.

Adv Chronic Kidney Dis. 2007;14(1):3-12.

16. Edvall CA. Renal function in hyperparathyroidism: a clinical study of 30 cases with special reference to selective

renal clearance and renal vein catheterization. Acta Chirur Scand Suppl. 1958;114(Suppl 229):1-56.

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