Original Article
Association of Hypokalemia, Aldosteronism, and Renal Cysts
N Engl J Med 1990; 322:345-351February 8, 1990
- Abstract
- Abstract
The recognition of renal cysts in two patients with chronic hypokalemia and the renal effects of hypokalemia in certain species of animals prompted this study of the possible association of hypokalemia and renal cysts in patients with primary aldosteronism or primary renal potassium wasting.
Using CT scans, we studied 55 patients with primary aldosteronism, of whom 24 had cysts (44 percent). The cysts were more frequent in patients with adrenal tumors than in those with idiopathic adrenal hyperplasia. Sixteen of the 26 patients with tumors (62 percent) had renal cysts, which were often multiple and located in the medulla. Lower plasma potassium levels and higher serum aldosterone levels, urinary aldosterone excretion, and plasma renin activity were correlated with the extent of the cystic disease. Sequential observations indicated that prolonged hypokalemia can be accompanied by the development of renal scarring and that the size and number of cysts can decrease markedly in some patients after the removal of an adrenal adenoma. The association of hypokalemia, aldosteronism, and renal cysts was also supported by the finding of multiple medullary cysts in two patients with primary renal potassium wasting.
We conclude that chronic hypokalemia is accompanied by enhanced renal cystogenesis and may lead to interstitial scarring and renal insufficiency. Renal cysts are thus dynamic structures whose growth can be influenced by hormonal or pharmacologic interventions. (N Engl J Med 1990; 322:345–51.)
Media in This Article
Figure 1
Abdominal CT Scans Obtained before (Panels a and b) and Four Years after (Panels c and d) the Removal of a Right Adrenal Adenoma in a Patient with Primary Aldosteronism (Patient 1).Figure 2
Plasma Potassium Level, Serum Aldosterone Level, and Plasma Renin Activity in Patients with Primary Aldosteronism with and without Renal Cysts at the Time of Evaluation at the Mayo Clinic.Article Activity
- Article
RENAL cysts arise from diverticula or segmental dilatations of the renal tubules that develop as part of the normal aging process.1 , 2 Many poorly understood genetic, environmental, and local factors can enhance the development of cysts and thus result in various renal cystic diseases. One such factor may be chronic hypokalemia. It is known to cause tubular hypertrophy and dilatation in some species of animals3 4 5 and may contribute to cyst formation under some experimental conditions.6 We recently studied two patients with primary aldosteronism who had prolonged, profound hypokalemia and renal cystic disease, in whom the number and size of cysts decreased markedly after the removal of an adrenal adenoma. These findings prompted us to study the frequency and clinical correlates of renal cysts in the patients with primary aldosteronism seen at our institution. To determine whether the findings in the patients with primary aldosteronism were unique to this form of chronic hypokalemia, we also studied a group of patients with primary renal potassium wasting.
Methods
Patients with Primary Aldosteronism
Between 1957 and 1986, 262 patients with primary aldosteronism were seen at the Mayo Clinic. This diagnosis was based on the presence of the following: hypertension, hypokalemia with inappropriate kaliuresis, increased 24-hour urinary aldosterone excretion, low plasma renin activity, and normal glucocorticoid secretion.7 The tests and methods used to identify the subtype of primary aldosteronism included adrenal computed tomography (CT), the responses of the serum aldosterone concentration to upright posture, and adrenal iodocholesterol scintigraphy.7 Eighty of these patients had abdominal CT scans available for review; the scans were limited to the adrenal glands in 25 patients and included both entire kidneys in 55, 34 of whom (62 percent) underwent CT after the intravenous administration of contrast material. Among these 55 patients, 24 had an aldosterone-producing adenoma, 29 had idiopathic hyperaldosteronism with bilateral adrenal hyperplasia, and 2 had aldosterone-producing adrenocortical carcinomas. The findings on the CT scans in these 55 patients were compared with those in a control group of 110 patients with essential hypertension. For every patient with primary aldosteronism, two patients with essential hypertension were matched according to sex, age, and year of examination. Among the 110 patients with essential hypertension, 76 (69 percent) underwent CT after the intravenous administration of contrast material. In addition, the findings on the CT scans in the patients with primary aldosteronism were compared with those in two groups of patients who had undergone CT scanning mainly for disorders unrelated to the urinary tract (historical controls).8 , 9 In the study by Laucks and McLachlan,8 10-mm cross-sectional slices of both kidneys were obtained before and after the intravenous administration of contrast material. In the study by Tada et al.,9 8-mm slices were obtained after the intravenous administration of contrast material, but some kidneys were not evaluated in their entirety. To determine whether the decrease in the size and number of cysts that occurred after the correction of the hypokalemia in Patients 1 and 2 was common, follow-up CT scanning was done in five additional patients with primary aldosteronism who had deep-seated medullary cysts.
Patients with Primary Renal Potassium Wasting
Between 1984 and 1989, the diagnosis of primary renal potassium wasting was confirmed in 15 patients seen at the renal function laboratory of the Mayo Clinic. This diagnosis was based on the presence of the following: chronic hypokalemic metabolic alkalosis with normal blood pressure, inappropriate kaliuresis, increased urinary chloride excretion, and negative screening tests for diuretic drugs in the urine. Five of these patients had available for review abdominal CT scans that included both entire kidneys. The diagnosis of hypokalemia had been established before CT scanning in all 15 patients.
Laboratory Methods
Serum creatinine and plasma electrolyte concentrations were determined by standard techniques. Serum aldosterone levels, urinary aldosterone excretion, and plasma renin activity were determined by radioimmunoassay.10 The blood samples for the determinations of the serum aldosterone level and plasma renin activity were obtained after the patient had been in the upright position for at least two hours and at least one week after the withdrawal of all antihypertensive medication, with the exception of guanethidine, guanadrel, or prazosin in some patients.
Statistical Analysis
The rank-sum test and the chi-square test were used to compare the results in the groups of patients with primary aldosteronism with and without cysts. Rank correlations were calculated to assess the degree of association between various measurements and the presence and extent of renal cysts.11 Stepwise logistic regression analysis and stepwise multiple regression analysis with backward elimination of variables that did not achieve a P value of 0.05 were used to assess the ability of the variables to predict the presence or absence of cysts and the extent of the cystic involvement as reflected by a rank given to each patient on the basis of the number and location of the cysts.12 , 13 Patients with deep-seated medullary cysts were given a higher rank than those with only superficial cortical cysts. Within each subgroup, the patients were ranked according to the number of cysts. All reported P values are two-tailed. All P values below 0.05 were considered to indicate statistical significance.
Results
Findings in Patients with Primary Aldosteronism
The case histories of the first two patients with primary aldosteronism and renal cysts were as follows.
Patient 1 was found to have hypertension in 1976 at the age of 31. He was treated initially with hydrochlorothiazide and triamterene. He began to feel weak in 1980, and in September 1981 he was hospitalized elsewhere after a near-paralytic collapse, at which time his plasma potassium level was 1.5 mmol per liter. The drugs were discontinued, and he was treated with potassium chloride (80 mmol daily).
He was first evaluated at our institution in February 1982. He was taking no antihypertensive medication, and his blood pressure was 175/110 mm Hg. The results of his laboratory tests then and later are shown in Table 1Table 1
Laboratory Data on Two Patients with Primary Aldosteronism.. Urinary glucocorticoid excretion was normal. Bolus nephrotomography showed multiple cysts distorting the collecting system in both kidneys and a mass in the right adrenal gland. CT of the abdomen confirmed the presence of a 2-cm right adrenal mass and multiple bilateral cysts, primarily in the medullary regions of both kidneys (Fig. 1Figure 1Abdominal CT Scans Obtained before (Panels a and b) and Four Years after (Panels c and d) the Removal of a Right Adrenal Adenoma in a Patient with Primary Aldosteronism (Patient 1).a and 1b). No evidence of polycystic kidney disease was found in other members of his family.At operation, a right adrenal adenoma, measuring 2.3 by 2.2 by 1.5 cm, was removed. Two months later, the patient's blood pressure was 125/90 mm Hg. He returned for evaluation four years later, at which time he was taking 10 to 12 antacid tablets (calcium carbonate; Tums) daily for dyspepsia. His blood pressure was 160/110 mm Hg. CT of the abdomen revealed multiple parenchymal calcifications of various sizes in the medullary regions of both kidneys and multiple parenchymal scars in both kidneys (Fig. 1c). After the intravenous administration of contrast medium (Fig. 1d), CT revealed one cyst in the upper pole and several small cysts in the lower pole of the right kidney and in the midportion of the left kidney. As compared with the CT scan obtained in 1982, the more recent scan showed that the number and size of the medullary cysts were markedly decreased. The antacid tablets were discontinued, and nifedipine therapy was started for the hypertension.
Patient 2 was found to have hypertension in 1957 at the age of 29. She had subsequently taken a number of different antihypertensive medications, including thiazides, but her blood pressure was never well controlled. In 1974, she began to feel weak while she was walking or climbing stairs. Her plasma potassium value was reportedly very low. Thiazide therapy was discontinued, and she was hospitalized for parenteral potassium replacement.
She came to our institution in May 1974. At that time, her blood pressure was 210/130 mm Hg. Laboratory values are shown in Table 1. Her serum calcium level was 2.7 mmol per liter, and her serum parathyroid hormone level was 190 ml-eq per liter (normal, ≤50). Excretory urography revealed multiple bilateral renal calculi in the papillary tips and bilateral parenchymal cysts. Intravenous bolus nephrotomography confirmed the presence of bilateral cysts and revealed a left adrenal mass. At operation, a left adrenal adenoma, measuring 3.0 by 2.5 by 2.5 cm, was removed. Two weeks later, a left inferior parathyroid adenoma was removed.
When the patient was reevaluated one year later, her blood pressure was 165/110 mm Hg. Excretory urography revealed a decrease in the size of the kidneys and of at least one of the cysts. Bilateral selective renal angiography confirmed the presence of bilateral cysts. Many of the cysts were located in the medullary regions and were associated with splaying of the arcuate vessels. Because of the multiple bilateral renal cysts, a diagnosis of polycystic kidney disease was considered. Family screening revealed no other family members with renal cysts. The patient was treated with propranolol, hydralazine, and a thiazide diuretic for hypertension. She returned 12 years later for reevaluation (Table 1). A CT scan of the abdomen revealed medullary calcifications, focal renal scars, and residual bilateral medullary and cortical cysts.
Among the 55 patients with primary aldosteronism, 24 (44 percent) had renal cysts (Table 2Table 2
Frequency of Cysts in Patients with Primary Aldosteronism, Patients with Essential Hypertension, and Historical Controls.). In contrast, 27 of the 110 control patients with essential hypertension (25 percent) had renal cysts. The frequency of renal cysts was 23 percent among the historical controls described in the literature.8 , 9 Among the 24 patients with primary aldosteronism who had cysts, the mean number of cysts was 5 (range, 1 to 22), as compared with 2 cysts (range, 1 to 11) in the 27 patients with essential hypertension who had cysts and with 1 and 2 cysts in the 127 patients who had cysts in the two studies of unselected patients.8 , 9 Table 3Table 3
Clinical and Laboratory Findings in Patients with Primary Aldosteronism, According to the Presence or Absence of Renal Cysts.* shows the sex, age, duration of hypertension, lowest recorded plasma potassium level, blood pressure, serum aldosterone and creatinine levels, plasma potassium level, rate of urinary excretion of aldosterone, and subtype of primary aldosteronism in the 24 patients who had renal cysts and the 31 patients who did not. The patients with cysts had slightly more severe hypokalemia, in terms of both the lowest recorded plasma potassium value and that recorded at the time of evaluation, higher levels of both serum aldosterone and plasma renin activity (Fig. 2Figure 2Plasma Potassium Level, Serum Aldosterone Level, and Plasma Renin Activity in Patients with Primary Aldosteronism with and without Renal Cysts at the Time of Evaluation at the Mayo Clinic.), a higher frequency of adrenal tumors, and a lower frequency of idiopathic hyperaldosteronism. Sixteen of the 26 patients (62 percent) with adrenal tumors and 8 of the 29 patients (28 percent) with idiopathic hyperaldosteronism with bilateral adrenal hyperplasia had renal cysts.In 10 of the 24 patients with cysts, the cysts were situated predominantly or exclusively in the renal medulla. The remaining 14 patients had cortical cysts only. As compared with the patients who had cortical cysts, those with medullary cysts had a higher mean number (±SD) of cysts (9±7 vs. 2±1; P<0.001; Fig. 3Figure 3
Number of Renal Cysts in Each of the 55 Patients with Primary Aldosteronism.) and a higher frequency of adrenal tumors (9 of 10 vs. 7 of 14 patients; P = 0.040 by chi-square test, P = 0.079 by Fisher's exact test).The extent of cystic involvement correlated negatively with the lowest plasma potassium level (r = −0.28, n = 54, P = 0.044) and the initial plasma potassium level (r = −0.39, n = 55, P = 0.003) and positively with the serum aldosterone level (r = 0.47, n = 29, P = 0.010), the urinary excretion of aldosterone (r = 0.27, n = 54, P = 0.045), and surprisingly, plasma renin activity (r = 0.30, n = 55, P = 0.026). The extent of cystic involvement was significantly greater in the 24 patients with adrenal adenomas than in the 29 patients with idiopathic hyperaldosteronism with bilateral adrenal hyperplasia (P = 0.024). Logistic regression analysis showed that lower plasma potassium levels (P = 0.008) and higher plasma renin activity (P = 0.015) at the time of the metabolic evaluation were independently predictive of the presence of cysts. These variables remained predictive of the presence of cysts (P = 0.011 and 0.014, respectively) after the two patients with adrenal carcinomas were excluded from the analysis. Multiple linear regression analysis showed that lower plasma potassium levels (P = 0.003), increased urinary excretion of aldosterone (P = 0.016), and higher plasma renin activity (P = 0.016) were simultaneously predictive of more severe cystic involvement.
In addition to Patients 1 and 2, follow-up CT scans were obtained in four other patients with medullary cysts and in one additional patient with a large adrenal adenoma and profound hypokalemia who was seen after the completion of the study. These follow-up studies were done 35 months (range, 6 to 55) after adrenal surgery in three patients and spironolactone therapy in two. Among the five patients studied after treatment, cyst regression was observed in only one, in a study done six months after the removal of an adrenal adenoma measuring 5.0 by 4.5 by 3.5 cm. The four remaining patients with medullary cysts could not be studied: the two patients with adrenal carcinoma had died, and two patients chose not to participate.
Findings in Patients with Primary Renal Potassium Wasting
Three of the five patients with primary renal potassium wasting who had CT scans available for review had renal cysts. The median age of these five patients was 34 years (range, 30 to 49). One patient had only two small cysts in the cortical and corticomedullary regions. The other two (Patients 3 and 4) had multiple deep-seated medullary cysts. The laboratory values for Patients 3 and 4 are summarized in Table 4Table 4
Laboratory Data on Two Patients with Primary Renal Potassium Wasting., and a brief description of these two patients follows.Patient 3 was a 30-year-old man with a two-year history of weakness who was found to have a plasma potassium level of 1.8 mmol per liter in 1984 after two weeks of diarrhea and vomiting. A stool culture was positive for Campylobacter jejuni, and the diarrhea subsided after two days of oral erythromycin therapy. Despite treatment with oral potassium chloride, his plasma potassium levels remained in the range of 2.0 to 3.0 mmol per liter.
He was initially evaluated at our institution in August 1984. His blood pressure was 124/62 mm Hg when he was supine and 112/70 mm Hg when he was standing. His laboratory test results then and later are shown in Table 4. The serum magnesium level was 0.58 mmol per liter (normal range, 0.70 to 0.86), and the rate of urinary excretion of magnesium was 6.8 mmol per 24 hours. CT of the abdomen revealed normal adrenal glands and slightly increased attenuation at the corticomedullary junction of each kidney (Fig. 4Figure 4
Abdominal CT Scans Obtained after the Intravenous Administration of Contrast Material before (Panels a and b) and Four Years after (Panels c and d) the Diagnosis of Primary Renal Potassium Wasting in Patient 3.a and 4b). Tomography revealed a tiny calculus in the upper pole of the left kidney, and excretory urography showed very mild precaliceal ectasia in several papillae. The diagnosis was primary renal potassium and magnesium wasting. Treatment with potassium chloride (120 to 160 mmol daily) and magnesium oxide (500 mg twice daily) was begun.The patient returned for reevaluation one, three, and four years later. In July 1987, renal ultrasonography revealed bilateral renal cysts, and spironolactone (50 mg three times a day) was added to his treatment regimen. One year later, the presence of deep-seated medullary cysts was confirmed by CT (Fig. 4c and 4d).
The family history revealed that one brother also had hypokalemia. His parents, a sister, and two children had normal plasma potassium concentrations. Another brother and one child have not been evaluated.
Patient 4 was found to have a plasma potassium level of 2.9 mmol per liter during an evaluation for atypical chest pain in 1984 at the age of 39. The presence of hypokalemia was confirmed on several occasions between 1984 and 1988, but he was given potassium chloride for brief periods only.
The patient was first seen at our institution in April 1989. His blood pressure was 128/80 mm Hg while he was seated. Laboratory values are shown in Table 4. CT of the abdomen revealed normal adrenal glands and multiple deep-seated medullary renal cysts. The diagnosis was primary renal potassium wasting, and treatment with potassium chloride (48 mmol daily) and triamterene (50 mg four times daily) was begun. After two months of therapy, the plasma potassium level was 3.4 mmol per liter. There was no family history of hypokalemia.
Discussion
The association of hypokalemia, aldosteronism, and renal cysts in patients with primary aldosteronism is supported by the decrease in the size and number of the cysts that occurred after the removal of an adrenal adenoma in some patients; the finding that among patients with primary aldosteronism, those who had renal cysts had lower plasma potassium levels, higher serum aldosterone levels, and increased urinary excretion of aldosterone as compared with those who did not have renal cysts; and the finding of a higher frequency of renal cysts in the patients with primary aldosteronism than in a control group of patients with essential hypertension or in historical controls8 , 9 studied by contrast-enhanced CT (Table 2). In addition, the association of hypokalemia, aldosteronism, and renal cysts is supported by the observations in two patients with primary renal potassium wasting, chronic hypokalemia, and elevated plasma renin activity, serum aldosterone levels, and urinary aldosterone excretion in whom multiple cysts were present initially or were observed during follow-up — a pattern similar to that observed in some patients with primary aldosteronism.
Hellman et al.14 described a patient who had primary aldosteronism, primary hyperparathyroidism, and sponge kidney with renal enlargement. Saeki et al.15 reported the association of primary aldosteronism and autosomal dominant polycystic kidney disease in one patient. In our first two patients with primary aldosteronism (Patients 1 and 2), the renal cysts were located primarily in the renal medulla. Neither of these patients had sponge kidney, and none of our patients had a family history of polycystic kidney disease.
The associations that we found should be interpreted within the context of what is known about the pathogenesis of cysts and about the effect of hypokalemia on the kidney. A critical factor in cyst formation is the enhanced growth and proliferation of the epithelial cells lining the cysts.2 Under various experimental conditions, a decrease in the extracellular potassium concentration or an increase in the intracellular potassium concentration stimulates protein synthesis, cell division, or both.16 17 18 A decrease in the potassium concentration in the medium stimulates the proliferation of African green monkey kidney cells in culture.16 In rodents, hypokalemia causes hyperplasia of the collecting-tubule cells in the outer medulla that is sufficient to obstruct the tubular lumen, resulting in tubular dilatation proximal to the hyperplasia and renal enlargement.3 4 5 Renal cysts develop in newborn rabbits, hamsters, and rats that are given long-acting corticosteroids, and the cysts may6 , 19 or may not20 be accompanied by severe hypokalemia. The development of these cysts can be prevented by the administration of potassium chloride.6 , 20 On the basis of these studies, it seems likely that the profound and prolonged hypokalemia observed in some patients with primary aldosteronism or with potassium-wasting disorders may facilitate the development of renal cysts by affecting the proliferation of tubular epithelial cells.
An unexpected finding is the positive correlation between plasma renin activity and the presence and extent of renal cysts in patients with primary aldosteronism. Because the patients with primary aldosteronism who had renal cysts had the lowest plasma potassium values and the highest serum aldosterone values and urinary aldosterone-excretion rates, they would have been expected to have more marked suppression of the renin—angiotensin system and, therefore, lower plasma renin activity. Perhaps the plasma renin activity in these patients came from sources other than the renal vasculature and the juxtaglomerular apparatus, such as the tubular epithelial cells,21 the adrenal gland,22 or the adrenal tumors.23 , 24 Although intrarenal angiotensin II may enhance the development of cysts in rats fed diphenylthiazole,25 the plasma renin activity in the patients with primary aldosteronism and renal cysts was so low that such an effect of angiotensin II on the development of renal cysts induced by hypokalemia seems unlikely.
The renal scarring observed after prolonged hypokalemia and the decrease in the number and size of the renal cysts after correction of the hypokalemia deserve special comment. Whether or not prolonged potassium depletion leads to permanent renal damage in humans has been controversial. In a large series of patients with chronic hypokalemia due to laxative or diuretic abuse, interstitial fibrosis was found in the majority.26 It has recently been proposed that increased cortical ammonia levels contribute to hypokalemic nephropathy through ammonia-mediated activation of the alternative complement pathway.27 In our Patients 1 and 2, renal scars developed despite the correction of chronic hypokalemia and the improvement or stabilization of renal function. The reversal of cystic disease after removal of a cystogen in laboratory animals28 and after the modification of culture conditions in tissue-culture models29 is well documented. The disappearance of renal cysts after the correction of a metabolic disorder in humans is not unique. The reversal of uremia-acquired renal cystic disease can occur after renal transplantation.30 These observations give further support to the concept that renal cysts are dynamic structures whose growth can be influenced or even reversed by pharmacologic measures.
We are indebted to Dr. D.M. Wilson for help in the preparation of the manuscript.
Source Information
From the Division of Nephrology and Internal Medicine (V.E.T.), the Division of Endocrinology, Metabolism, and Internal Medicine and the Division of Hypertension (W.F.Y.), the Section of Biostatistics (K.P.O.), and the Department of Diagnostic Radiology (R.R.H.), Mayo Clinic and Mayo Foundation, Rochester, MN 55905. Address reprint requests to Dr. Torres at the Mayo Clinic, 200 First St. SW, Rochester, MN 55905.
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