Chronic hypokalemic nephropathy: A clinical study

Bock, K. D.; Cremer, Wolfgang; Werner, Ulrike

doi:10.1007/bf01477459

Cited by 22 publications

(23 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Pere et al (29,30) reported that a high-potassium diet (2.4% potassium) is renoprotective in cyclosporine-induced nephrotoxicity, compared with a diet containing 0.8% potassium. In contrast, chronic potassium depletion causes renal functional deterioration, interstitial nephritis, or cyst formation in animals and humans (3,4,6,11,32,34,40,47). The proposed underlying mechanisms of the deleterious effect of potassium depletion include activation of the local renin-angiotensin II system (RAS) (32), increased angiotensin II receptor (AT 1 ) expression (12), and altered activity of the sodium-potassium pump in the renal tubule (35), acting by blood pressure-dependent and/or blood pressureindependent mechanisms.…”

mentioning

confidence: 99%

Renal inflammation is modulated by potassium in chronic kidney disease: possible role of Smad7

Wang¹,

Soltero²,

Zhang³

et al. 2007

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

High-potassium diets have been shown to be beneficial in cardiovascular disease partly because of a blood pressure-lowering effect. The effect of potassium on inflammation has not been studied. We investigated the influence of potassium supplementation on the degree of renal inflammation and the intracellular signaling mechanisms that could mediate inflammation in chronic kidney disease (CKD). CKD was created in male SpragueDawley rats by subtotal nephrectomy. Two groups of CKD rats were pair fed with diets containing 2.1% potassium (potassium-supplemented diet) or 0.4% potassium (basal diet). Body weight, blood pressure, and blood and urine electrolytes were measured biweekly. The animals were euthanized at week 8, and the remnant kidneys were analyzed by histology, immunohistochemistry, Western blotting, and real-time quantitative PCR. In the CKD pair-fed groups, blood potassium concentration did not differ significantly, but blood pressure was lower in the potassium-supplemented group. Compared with the basal diet, potassium supplementation decreased renal tubulointerstitial injury and suppressed renal inflammation as evidenced by decreased macrophage infiltration, lower expression of inflammatory cytokines, and decreased NF-B activation. These renoprotective effects were associated with downregulation of renal transforming growth facto-␤, upregulation of renal Smad7, and lower blood pressure. Our results show that potassium supplementation can reduce renal inflammation and hence, could modulate the progression of kidney injury in CKD.NF-B; potassium; Smad7; TGF-␤ THE MEDIATORS OF PROGRESSIVE chronic kidney disease (CKD) remain largely unsolved, especially the mechanisms leading to progressive fibrosis of the kidney. The presence of fibrosis in the kidney is generally preceded by glomerular and tubulointerstitial infiltration by inflammatory cells. It is likely that the infiltrating inflammatory cells activate NF-B, leading to the production and release of proinflammatory cytokines and adhesion molecules (e.g., IL-1␤, ICAM-1) as well as profibrotic cytokines [e.g., transforming growth factor (TGF)-␤]. The consequence is renal inflammation and progressive fibrosis of the kidney, leading to loss of function. Treatment strategies have included medications and dietary modifications such as limitation of protein and sodium intake to reduce the accumulation of potential uremic toxins and blood pressure. The potential influence of potassium intake on progressive kidney disease remains largely unknown.There are indications that potassium supplementation may be beneficial in cardiovascular diseases, especially for problems arising as a complication of hypertension (7,17,20,27,38). There are also indications that potassium supplementation might reduce local vascular inflammatory reactions. Ishimitsu et al. (16) reported that potassium supplementation suppressed macrophage activity in stroke-prone spontaneously hypertensive rats (SHPsp). In their study, the rats were fed a normal or high-potassium diet, and excised aort...

show abstract

mentioning

confidence: 99%

Renal inflammation is modulated by potassium in chronic kidney disease: possible role of Smad7

Wang¹,

Soltero²,

Zhang³

et al. 2007

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

show abstract

“…Renal insufficiency in eating disorders has been reported to be induced by hypokalemia relevant to vomiting or laxative abuse (Bock et al, 1978;Copeland, 1994;Ishikawa et al, 1999;Riemenschneider & Bohle, 1983;Tsuchiya et al, 1995). The initial biopsy (1977) showed juxtaglomerular hyperplasia, and repeated biopsy (2001) showed interstitial nephritis and proximal tubular swelling.…”

Section: Resultsmentioning

confidence: 94%

“…However, few studies have revealed the extent of renal damage, especially morphologic changes, over long-term bulimic symptoms (Bock et al, 1978;Copeland, 1994;Riemenschneider & Bohle, 1983;Tsuchiya et al, 1995). To our knowledge, this is the first case report of a patient with longstanding bulimia nervosa and an eventual ''end-stage kidney'' characterized by hypokalemic nephropathy and diffuse glomerulosclerosis.…”

Section: Resultsmentioning

confidence: 96%

“…Many medical complications associated with abnormal eating habits exist, including disturbances in gastrointestinal, metabolic, endocrine, and renal function (Fairburn & Harrison, 2003). In particular, renal function has been reported to be impaired even in the short term by severe energy restriction in anorexia nervosa, and by binge/purges in bulimia nervosa (Bock, Cremer, & Werner, 1978;Copeland, 1994;Riemenschneider & Bohle, 1983;Ishikawa et al, 1999;Sharp & Freeman, 1993;Tsuchiya, Nakauchi, Hondo, & Nihei, 1995;). However, little is known about the extent of renal damage over long-term binge/purges.…”

Section: Introductionmentioning

confidence: 95%

See 1 more Smart Citation

“End-stage kidney” in longstanding bulimia nervosa

Yasuhara

Naruo

Taguchi

et al. 2005

Int. J. Eat. Disord.

View full text Add to dashboard Cite

Over the following 26 years, the patient's eating behaviors remained chaotic, and her renal function gradually deteriorated. After the patient died of pneumonia and sepsis at age 52 years, autopsy of her kidney showed chronic interstitial nephritis, proximal tubular swelling, and diffuse glomerular sclerosis, suggesting chronic glomerular injury associated with long-term binge/purges. To our knowledge, this is the first case report of a patient with BN with long-term binge/purges who developed an eventual "end-stage kidney" characterized by hypokalemic nephropathy and diffuse glomerulosclerosis.

show abstract

“…Hypokalemia and chronic dehydration, caused by laxative and/or diuretic abuse and chronic fluid restriction, appear to be the most likely mechanisms for the development of these conditions. Bock, Cremer, and Werner (1978) reported on a series of 23 patients with chronic hypokalemia, renal insufficiency, and eating disorders, showing secondary interstitial nephritis in the 9 patients for whom biopsy material was available. Low protein intake may play a role by causing a decrease in the glomerular filtration rate (GFR; Ichikawa, Purkerson, & Klahr, 1980).…”

Section: Resultsmentioning

confidence: 98%