- Email: [email protected]
Snoring and Sleepiness
925
sleep, morning headaches, depression, loss of libido, enuresis, and hallucinations at sleep onset.’° Around 90% of patients are male-which may reflect the apnoea-promoting effect of testosterone II -and around 60% are obese. 10 Medical sequelae include arrhythmias during apnoeas, but their clinical importance is
Snoring and Sleepiness SINCE pathological
sleepiness and snoring were first
ago’ the has been widely diagnosed in sleep apnoea syndrome North America, continental Europe, and Australasia and is now thought to affect perhaps 1 % of adults. 2,3 In Britain the diagnosis is rarely made and, in view of the frequency of sleep apnoea syndrome in patients of British descent in North America and Australasia, is probably much overlooked. On inspiration, the pharynx remains patent only because of contraction of airway-opening muscles. These are true respiratory muscles whose activity varies with respiration and increases when ventilation increases.4 During sleep the tone in these muscles declines and the airway may narrow. If the narrowing is subcritical, snoring results; when the airway closes, apnoea occurs. After an interval, the apnoea leads to arousal, which raises upper-airway-opening muscle tone-whereupon the patient takes a few grunting, snoring breaths before falling asleep again and becoming apnoeic once more. The repeated cycle of apnoea and arousal disrupts sleep, producing the typical daytime somnolence. The sleep apnoea syndrome is usually defined as the occurrence of more than five 10-second apnoeas per hour of sleep,5 but this means that the label can be attached to many middle-aged and elderly people who are entirely without symptoms.6-9 A better definition would be the coexistence of fifteen apnoeas per hour of sleep with supporting symptoms. The dominant symptoms are excessive daytime sleepiness and loud snoring. The recurrent dozing results in disruption of life at work and at home, as well as dangers to the patient and other people: falling asleep while driving is a particular hazard. Other features may include restless linked to apnoeas during sleep twenty years
unclear.’2 The condition may progress to the classical Pickwickian syndrome with daytime hypoxia and hypercapnia. Polycythaemia and cor pulmonale are most likely to develop in patients who have both sleep I apnoea and lung disease. 13 It is now clear that patients with the sleep apnoea syndrome have abnormal upper airways with floppy pharyngeal walls even when awake.’4 Most also have pharyngeal narrowing the cause of which is probably not fat deposition.’S The combination of narrowing and increased compliance of the upper airway predisposes to pharyngeal collapse.l8 There is no evidence that apnoeas are caused by a selective decrease in upper-airway-opening muscle tone during sleep in patients with sleep apnoea.18,19 Narrowing of the nasopharyngeal airway-eg, by tonsillar or adenoidal enlargement-will increase the suck pressure required to inspire and thus predispose to upper airway collapse. Other conditions associated with sleep apnoea include retrognathia, hypothyroidism, acromegaly, and hypertension.20,21 The clinical importance of the association with hypertension is unclear. Sleep apnoea can often be diagnosed by observation, but it cannot be excluded by observation.22 Useful screening tests include electrocardiographic monitoring to detect bradycardia associated with each apnoea23 and overnight ear oximetry. However, to assess the frequency of apnoeas and arousals and the severity of the hypoxia, or to exclude the diagnosis, overnight monitoring of breathing patterns, oxygenation, and electroencephalogram is required. Indications for 11. Sandblom RE, Matsumoto AM, Schoene RB, et al. Obstructive sleep apnea syndrome induced by testosterone administration. N Engl J Med 1983; 308: 508-10. 12. Miller WP. Cardiac arrhythmias and conduction disturbances in the sleep apnea syndrome: prevalence and significance. Am J Med 1982; 73: 317-21. 13. Bradley TD, Rutherford R, Grossman RF, et al. Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome. Am Rev Respir Dis 1985, 131: 835-39. 14. Brown IG, Bradley TD, Phillipson EA, Zamel N, Hoffstein V. Pharyngeal compliance in snoring subjects with and without obstructive sleep apnea. Am Rev Respir Dis
1985; 132: 211-15. 15.
H, Tassinari CA, Polygraphic study of the episodic diurnal and nocturnal (hypnic and respiratory) manifestation of the Pickwick syndrome. Brain Res 1966; 2: 167-86. 2. Franceschi M, Zamproni P, Crippa D, Smirne S. Excessive daytime sleepiness: a 1 year study in an unselected in-patient population. Sleep 1982; 5: 239-47. 3. Lavie P. Incidence of sleep apnea in a presumably healthy, working population: a significant relationship with excessive daytime sleepiness. Sleep 1983; 6: 312-18. 4. Onal E, Lopata M, O’Connor TD. Diaphragmatic and genioglossal electromyogram responses to isocapnic hypoxia in humans. Am Rev Respir Dis 1981; 124: 215-17. 5 Guilleminault C, van den Hoed J, Mitler M. Clinical overview of the sleep apnea syndrome. In: Guilleminault C, Dement W, eds. Sleep apnea syndromes. New York: Alan R Liss, 1978: 1-12. 1. Gastaut
6
Duron B.
Carskaddon MA, Dement WC. Respiration during sleep in the aged human. J Gerontol 1981, 36: 420-23.
7.
KreigerJ, Tirlot JC, Mangm P, Kurtz D. Breathing during sleep in normal young and elderly subjects: hypopneas, apneas and correlated factors. Sleep 1983; 6: 108-20. 8. Bixler EO, Kales A, Cadieux RJ, Vela-Bueno A, Jacoby JA, Soldatos CR. Sleep apneic activity in older healthy subjects J Appl Physiol 1985; 58: 1597-601. 9. Catterall JR, Calverley PMA, Shapiro CM, Flenley DC, Douglas NJ. Breathing and oxygenation during sleep are similar in normal men and normal women. Am Rev Respir Dis 1985; 132: 86-88. 10. Guilleminault C, Simmons FB, Motta J, et al. Obstructive sleep apnea syndrome and tracheostomy: long term follow-up experience.Arch Intern Med 1981; 141: 985-88.
Haponik EF, Smith PL, Bohlman ME, Allen RP, Goldman SM, Bleeker ER. Computerised tomography in obstructive sleep apnea. Am Rev Respir Dis 1983;
127: 221-26. 16. Rivlin J, Hoffstein
V, Kalbfleisch J, MacNicholas W, Zamel N, Bryan AC. Upper airway morphology in patients with idiopathic obstructive sleep apnea Am Rev Respir Dis 1984; 129: 355-60. 17. Hoffstein V, Zamel N, Phillipson EA. Lung volume dependence of pharyngeal crosssectional area in patients with obstructive sleep apnea. Am Rev Respir Dis 1984; 130: 175-78. FQ, Sullivan CE. Upper airway closing pressures in obstructive sleep apnea. J Appl Physiol 1984; 57: 520-27. 19. Onal E, Lopata M, O’Connor T. Pathogenesis of apneas in hypersomnia—sleep apnea syndrome. Am Rev Respir Dis 1982; 125: 167-74. 20. Kales A, Bixler EO, Cadieux RJ, et al. Sleep apnoea in a hypertensive population. Lancet 1984; ii: 1005-08. 21. Fletcher EC, De Behnke RD, Lovoi MS, Gorin AB. Undiagnosed sleep apnea in patients with essential hypertension Ann Intern Med 1985; 103: 190-95. 22. Haponik EF, Smith PL, Meyers DA, Bleeker ER. Evaluation of sleep-disordered breathing: Is polysomnography necessary. Am J Med 1984; 77: 671-77. 23. Guilleminault C, Connolly S, Winkle R, Melvin T, Tilkian A. Cyclical variation ofthe heart rate in sleep apnoea. Mechanisms and usefulness of 24 h electrocardiography as a screening technique. Lancet 1984; i: 126-31. 24 Kryger MH, Mezon BJ, Acres JC, West P, Brownell L. Diagnosis of sleep breathing disorders in a general hospital. Arch Intern Med 1982; 142: 956-58. 18. Issa
926
performing sleep studies include excessive sleepiness, apnoeas reported by bed partners, unexplained polycythaemia,24 and unexplained right heart failure. Patients with sleep apnoea syndrome should be encouraged to lose weight and should be referred to an and
throat
surgeon to exclude nasopharyngeal narrowing. Alcohol and sedatives are to be avoided since they relax upper-airway-opening muscles and thus increase apnoeas.25 Other measures nose,
ear,
usually required. Drugs are often disappointing. Protriptyline, the drug of choice, works both by stimulating upper-airway-opening muscles26 and by decreasing rapid eye movement sleep,27 during which apnoeas are longest. Unfortunately, anticholinergic are
side-effects tend to limit its use. Progesterone is less effective.211 The place of surgery is unclear and neither uvulopalatopharyngoplasty29 nor hyoidplasty can be advocated until indications and complications are clarified. Mandibular advancement can help in retrognathiall but remodelling may occur. Patients with severe symptoms or with severe hypoxia, those who drive, and those not helped by drugs may require continuous positive airway pressure at night. This increases the pressure within the upper airway, so preventing airway collapse, and may also work by stimulating nasal flow receptors 18 and by increasing lung volume. 17 The pressure required is determined in hospital and long-term treatment at home is acceptable to most hypersomnolent patients." Commercial systems cost between 900 and 2500 per patient. Tracheostomy has little or no role in the modern treatment of sleep apnoea. The sleep apnoea syndrome is a disabling but treatable condition with a wide range of presentations. Physicians will only make this diagnosis when they remember to inquire about sleepiness and snoring, questions most of us were not taught to ask in our routine history-taking.
A
Kidney to Spare?
results of renal cadaver transplantation are now very good-thanks to increasing experience, the use of kidneys from heartbeating donors, better tissue matching, pre-transplant blood transfusion, and immunosuppression with cyclosporin-the shortage of cadaver kidneys with a growing waiting list ensures that kidneys from living THOUGH the
25. Issa
long-term
FG, Sullivan CE. Upper airway closing pressure in snorers. J Appl Physiol 1984;
528-35. 26. Bonora M, St John
57:
WM, Bledsoe TA. Differential elevation by protriptyline and depression by diazepam of upper airway respiratory motor activity. Am Rev Respir
Dis 1985; 131: 41-45. 27. Brownell LG, West P, Sweatman P, Acres JC, Kreiger MH. Protriptyline in obstructive sleep apnea. N Engl J Med 1982; 307: 1037-42. 28. Orr WC, Imes NK, Martin RJ. Progesterone therapy in obese patients with sleep apnea. Arch Intern Med 1979; 139: 109-11. 29. Simmons FB, Guilleminault C, Silvestri R. Snoring and some obstructive sleep apnea can be cured by oropharyngeal surgery. Arch Otolaryngol 1983; 109: 503-07. 30. Kuo PC, West RA, Bloomguist DS, McNeil RW. The effect ofmandibular osteotomy in three patients with hypersomnia sleep apnea. Oral Surg 1979; 48: 385-92. 31. Sullivan CE, Issa FG, Berthon-Jones M, McCauley VB, Costas LVJ. Home treatment of obstructive sleep apnoea with continuous positive airway pressure applied through a nose-mask. Bull Eur Physiopathol Respir 1984; 20: 49-54.
related volunteer donors will continue to be used. (In some countries a market exists for kidneys bought from living non-related donors, and the Transplantation Society is sufficiently concerned to contemplate expulsion of any member involved in the buying and selling of organs.’ ) Can we be certain that, in taking a kidney from a living donor, we do no long-term harm? In rats, ablation of a critical mass of normal renal tissue causes progressive damage to the renal remnant, attributed by Brenner2 to hyperperfusion. There is some evidence that similar mechanisms operate in man: 70-80% loss of renal function (associated with 80-90% loss of renal parenchyma), irrespective of cause, is associated in most cases with relentless further deterioration, even when the original cause has been successfully treated. Fears on this score were fuelled by a report from Zucchelli3 on four highly selected patients who had undergone uninephrectomy for a non-nephritic disease some years earlier: biopsy of the remaining kidney, done for investigation of proteinuria, revealed focal segmental glomerulosclerosis. Human kidney donation at a stroke removes 50% of renal mass and 30% of function ; so is there a risk that, in the long-term, some volunteer kidney donors will themselves become victims of renal failure? Many sizeable series of long-term follow-ups of kidney donors have now been reported, extending over periods of up to 20 years. 1-8 If hyperfiltration were damaging to the remaining kidney in the donor we would expect to see a progressive rise in serum creatinine and a fall in creatinine clearance. Such findings did not materialise .Even in older donors the fall in creatinine clearance did not exceed that normally found with advancing years.8In these series there was no suggestion that donors enjoying a high protein intake,4,5,7 as judged from dietary records or from 24-hour urinary nitrogen detemination, had a higher creatinine level than those on more moderate protein intake. In most, but not all,s published series the average urinary protein excretion increased and pathological proteinuria developed in a few donors, particularly males,8but this was not associated with an abnormal urinary sediment5 or raised plasma creatinine.9 It has been suggested on genetic grounds that, since donors are usually first-degree relatives of recipients, an increased incidence of renal abnormality, 1. Council of the Transplantation Society. Commercialisation in transplastation. the problems and some guidelines for practice. Lancet 1985; ii: 715-16. 2. Brenner BM, Meyer TW, Hostetter TH. Dietary protein intake and the progressive nature of kidney disease: The role of haemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation and intrinsic renal disease. N EnglJ Med 1982; 307: 652-59. 3. Zucchelli P, Cagnoli L, Casanova S, Donini U, Pasquali S. Focal glomerulosclerosisin patients with unilateral nephrectomy. Kidney Int 1983; 24: 649-55. 4. Mathillas O, Attman PO, Aurell M, Blohmé I, Brynger H, Granerus G, Westberg G. Long-term outcome of renal function and proteinuria in kidney transplant donors Proc ED TA-ERA 1984; 21: 574-78. 5. Tapson JS, Marshall SM, Tisdall SR, Wilkinson R, Ward MK, Kerr DNS. Renal function and blood pressure after donor nephrectomy Proc EDTA-ERA 1984, 21: 580-87. 6. Hoitsma AJ, Paul LC, Van Es LA, Koene RAP. Long-term follow-up of living kidney donors. Neth J Med 1985; 28: 226-30. 7. Anderson CF, Velosa JA, Frohnert PP, et al. The risks of unilateral nephrectomy Status of kidney donors 10-20 years postoperatively. Mayo Clin Proc 1985; 60: 367-74.
sleep, morning headaches, depression, loss of libido, enuresis, and hallucinations at sleep onset.’° Around 90% of patients are male-which may reflect the apnoea-promoting effect of testosterone II -and around 60% are obese. 10 Medical sequelae include arrhythmias during apnoeas, but their clinical importance is
Snoring and Sleepiness SINCE pathological
sleepiness and snoring were first
ago’ the has been widely diagnosed in sleep apnoea syndrome North America, continental Europe, and Australasia and is now thought to affect perhaps 1 % of adults. 2,3 In Britain the diagnosis is rarely made and, in view of the frequency of sleep apnoea syndrome in patients of British descent in North America and Australasia, is probably much overlooked. On inspiration, the pharynx remains patent only because of contraction of airway-opening muscles. These are true respiratory muscles whose activity varies with respiration and increases when ventilation increases.4 During sleep the tone in these muscles declines and the airway may narrow. If the narrowing is subcritical, snoring results; when the airway closes, apnoea occurs. After an interval, the apnoea leads to arousal, which raises upper-airway-opening muscle tone-whereupon the patient takes a few grunting, snoring breaths before falling asleep again and becoming apnoeic once more. The repeated cycle of apnoea and arousal disrupts sleep, producing the typical daytime somnolence. The sleep apnoea syndrome is usually defined as the occurrence of more than five 10-second apnoeas per hour of sleep,5 but this means that the label can be attached to many middle-aged and elderly people who are entirely without symptoms.6-9 A better definition would be the coexistence of fifteen apnoeas per hour of sleep with supporting symptoms. The dominant symptoms are excessive daytime sleepiness and loud snoring. The recurrent dozing results in disruption of life at work and at home, as well as dangers to the patient and other people: falling asleep while driving is a particular hazard. Other features may include restless linked to apnoeas during sleep twenty years
unclear.’2 The condition may progress to the classical Pickwickian syndrome with daytime hypoxia and hypercapnia. Polycythaemia and cor pulmonale are most likely to develop in patients who have both sleep I apnoea and lung disease. 13 It is now clear that patients with the sleep apnoea syndrome have abnormal upper airways with floppy pharyngeal walls even when awake.’4 Most also have pharyngeal narrowing the cause of which is probably not fat deposition.’S The combination of narrowing and increased compliance of the upper airway predisposes to pharyngeal collapse.l8 There is no evidence that apnoeas are caused by a selective decrease in upper-airway-opening muscle tone during sleep in patients with sleep apnoea.18,19 Narrowing of the nasopharyngeal airway-eg, by tonsillar or adenoidal enlargement-will increase the suck pressure required to inspire and thus predispose to upper airway collapse. Other conditions associated with sleep apnoea include retrognathia, hypothyroidism, acromegaly, and hypertension.20,21 The clinical importance of the association with hypertension is unclear. Sleep apnoea can often be diagnosed by observation, but it cannot be excluded by observation.22 Useful screening tests include electrocardiographic monitoring to detect bradycardia associated with each apnoea23 and overnight ear oximetry. However, to assess the frequency of apnoeas and arousals and the severity of the hypoxia, or to exclude the diagnosis, overnight monitoring of breathing patterns, oxygenation, and electroencephalogram is required. Indications for 11. Sandblom RE, Matsumoto AM, Schoene RB, et al. Obstructive sleep apnea syndrome induced by testosterone administration. N Engl J Med 1983; 308: 508-10. 12. Miller WP. Cardiac arrhythmias and conduction disturbances in the sleep apnea syndrome: prevalence and significance. Am J Med 1982; 73: 317-21. 13. Bradley TD, Rutherford R, Grossman RF, et al. Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome. Am Rev Respir Dis 1985, 131: 835-39. 14. Brown IG, Bradley TD, Phillipson EA, Zamel N, Hoffstein V. Pharyngeal compliance in snoring subjects with and without obstructive sleep apnea. Am Rev Respir Dis
1985; 132: 211-15. 15.
H, Tassinari CA, Polygraphic study of the episodic diurnal and nocturnal (hypnic and respiratory) manifestation of the Pickwick syndrome. Brain Res 1966; 2: 167-86. 2. Franceschi M, Zamproni P, Crippa D, Smirne S. Excessive daytime sleepiness: a 1 year study in an unselected in-patient population. Sleep 1982; 5: 239-47. 3. Lavie P. Incidence of sleep apnea in a presumably healthy, working population: a significant relationship with excessive daytime sleepiness. Sleep 1983; 6: 312-18. 4. Onal E, Lopata M, O’Connor TD. Diaphragmatic and genioglossal electromyogram responses to isocapnic hypoxia in humans. Am Rev Respir Dis 1981; 124: 215-17. 5 Guilleminault C, van den Hoed J, Mitler M. Clinical overview of the sleep apnea syndrome. In: Guilleminault C, Dement W, eds. Sleep apnea syndromes. New York: Alan R Liss, 1978: 1-12. 1. Gastaut
6
Duron B.
Carskaddon MA, Dement WC. Respiration during sleep in the aged human. J Gerontol 1981, 36: 420-23.
7.
KreigerJ, Tirlot JC, Mangm P, Kurtz D. Breathing during sleep in normal young and elderly subjects: hypopneas, apneas and correlated factors. Sleep 1983; 6: 108-20. 8. Bixler EO, Kales A, Cadieux RJ, Vela-Bueno A, Jacoby JA, Soldatos CR. Sleep apneic activity in older healthy subjects J Appl Physiol 1985; 58: 1597-601. 9. Catterall JR, Calverley PMA, Shapiro CM, Flenley DC, Douglas NJ. Breathing and oxygenation during sleep are similar in normal men and normal women. Am Rev Respir Dis 1985; 132: 86-88. 10. Guilleminault C, Simmons FB, Motta J, et al. Obstructive sleep apnea syndrome and tracheostomy: long term follow-up experience.Arch Intern Med 1981; 141: 985-88.
Haponik EF, Smith PL, Bohlman ME, Allen RP, Goldman SM, Bleeker ER. Computerised tomography in obstructive sleep apnea. Am Rev Respir Dis 1983;
127: 221-26. 16. Rivlin J, Hoffstein
V, Kalbfleisch J, MacNicholas W, Zamel N, Bryan AC. Upper airway morphology in patients with idiopathic obstructive sleep apnea Am Rev Respir Dis 1984; 129: 355-60. 17. Hoffstein V, Zamel N, Phillipson EA. Lung volume dependence of pharyngeal crosssectional area in patients with obstructive sleep apnea. Am Rev Respir Dis 1984; 130: 175-78. FQ, Sullivan CE. Upper airway closing pressures in obstructive sleep apnea. J Appl Physiol 1984; 57: 520-27. 19. Onal E, Lopata M, O’Connor T. Pathogenesis of apneas in hypersomnia—sleep apnea syndrome. Am Rev Respir Dis 1982; 125: 167-74. 20. Kales A, Bixler EO, Cadieux RJ, et al. Sleep apnoea in a hypertensive population. Lancet 1984; ii: 1005-08. 21. Fletcher EC, De Behnke RD, Lovoi MS, Gorin AB. Undiagnosed sleep apnea in patients with essential hypertension Ann Intern Med 1985; 103: 190-95. 22. Haponik EF, Smith PL, Meyers DA, Bleeker ER. Evaluation of sleep-disordered breathing: Is polysomnography necessary. Am J Med 1984; 77: 671-77. 23. Guilleminault C, Connolly S, Winkle R, Melvin T, Tilkian A. Cyclical variation ofthe heart rate in sleep apnoea. Mechanisms and usefulness of 24 h electrocardiography as a screening technique. Lancet 1984; i: 126-31. 24 Kryger MH, Mezon BJ, Acres JC, West P, Brownell L. Diagnosis of sleep breathing disorders in a general hospital. Arch Intern Med 1982; 142: 956-58. 18. Issa
926
performing sleep studies include excessive sleepiness, apnoeas reported by bed partners, unexplained polycythaemia,24 and unexplained right heart failure. Patients with sleep apnoea syndrome should be encouraged to lose weight and should be referred to an and
throat
surgeon to exclude nasopharyngeal narrowing. Alcohol and sedatives are to be avoided since they relax upper-airway-opening muscles and thus increase apnoeas.25 Other measures nose,
ear,
usually required. Drugs are often disappointing. Protriptyline, the drug of choice, works both by stimulating upper-airway-opening muscles26 and by decreasing rapid eye movement sleep,27 during which apnoeas are longest. Unfortunately, anticholinergic are
side-effects tend to limit its use. Progesterone is less effective.211 The place of surgery is unclear and neither uvulopalatopharyngoplasty29 nor hyoidplasty can be advocated until indications and complications are clarified. Mandibular advancement can help in retrognathiall but remodelling may occur. Patients with severe symptoms or with severe hypoxia, those who drive, and those not helped by drugs may require continuous positive airway pressure at night. This increases the pressure within the upper airway, so preventing airway collapse, and may also work by stimulating nasal flow receptors 18 and by increasing lung volume. 17 The pressure required is determined in hospital and long-term treatment at home is acceptable to most hypersomnolent patients." Commercial systems cost between 900 and 2500 per patient. Tracheostomy has little or no role in the modern treatment of sleep apnoea. The sleep apnoea syndrome is a disabling but treatable condition with a wide range of presentations. Physicians will only make this diagnosis when they remember to inquire about sleepiness and snoring, questions most of us were not taught to ask in our routine history-taking.
A
Kidney to Spare?
results of renal cadaver transplantation are now very good-thanks to increasing experience, the use of kidneys from heartbeating donors, better tissue matching, pre-transplant blood transfusion, and immunosuppression with cyclosporin-the shortage of cadaver kidneys with a growing waiting list ensures that kidneys from living THOUGH the
25. Issa
long-term
FG, Sullivan CE. Upper airway closing pressure in snorers. J Appl Physiol 1984;
528-35. 26. Bonora M, St John
57:
WM, Bledsoe TA. Differential elevation by protriptyline and depression by diazepam of upper airway respiratory motor activity. Am Rev Respir
Dis 1985; 131: 41-45. 27. Brownell LG, West P, Sweatman P, Acres JC, Kreiger MH. Protriptyline in obstructive sleep apnea. N Engl J Med 1982; 307: 1037-42. 28. Orr WC, Imes NK, Martin RJ. Progesterone therapy in obese patients with sleep apnea. Arch Intern Med 1979; 139: 109-11. 29. Simmons FB, Guilleminault C, Silvestri R. Snoring and some obstructive sleep apnea can be cured by oropharyngeal surgery. Arch Otolaryngol 1983; 109: 503-07. 30. Kuo PC, West RA, Bloomguist DS, McNeil RW. The effect ofmandibular osteotomy in three patients with hypersomnia sleep apnea. Oral Surg 1979; 48: 385-92. 31. Sullivan CE, Issa FG, Berthon-Jones M, McCauley VB, Costas LVJ. Home treatment of obstructive sleep apnoea with continuous positive airway pressure applied through a nose-mask. Bull Eur Physiopathol Respir 1984; 20: 49-54.
related volunteer donors will continue to be used. (In some countries a market exists for kidneys bought from living non-related donors, and the Transplantation Society is sufficiently concerned to contemplate expulsion of any member involved in the buying and selling of organs.’ ) Can we be certain that, in taking a kidney from a living donor, we do no long-term harm? In rats, ablation of a critical mass of normal renal tissue causes progressive damage to the renal remnant, attributed by Brenner2 to hyperperfusion. There is some evidence that similar mechanisms operate in man: 70-80% loss of renal function (associated with 80-90% loss of renal parenchyma), irrespective of cause, is associated in most cases with relentless further deterioration, even when the original cause has been successfully treated. Fears on this score were fuelled by a report from Zucchelli3 on four highly selected patients who had undergone uninephrectomy for a non-nephritic disease some years earlier: biopsy of the remaining kidney, done for investigation of proteinuria, revealed focal segmental glomerulosclerosis. Human kidney donation at a stroke removes 50% of renal mass and 30% of function ; so is there a risk that, in the long-term, some volunteer kidney donors will themselves become victims of renal failure? Many sizeable series of long-term follow-ups of kidney donors have now been reported, extending over periods of up to 20 years. 1-8 If hyperfiltration were damaging to the remaining kidney in the donor we would expect to see a progressive rise in serum creatinine and a fall in creatinine clearance. Such findings did not materialise .Even in older donors the fall in creatinine clearance did not exceed that normally found with advancing years.8In these series there was no suggestion that donors enjoying a high protein intake,4,5,7 as judged from dietary records or from 24-hour urinary nitrogen detemination, had a higher creatinine level than those on more moderate protein intake. In most, but not all,s published series the average urinary protein excretion increased and pathological proteinuria developed in a few donors, particularly males,8but this was not associated with an abnormal urinary sediment5 or raised plasma creatinine.9 It has been suggested on genetic grounds that, since donors are usually first-degree relatives of recipients, an increased incidence of renal abnormality, 1. Council of the Transplantation Society. Commercialisation in transplastation. the problems and some guidelines for practice. Lancet 1985; ii: 715-16. 2. Brenner BM, Meyer TW, Hostetter TH. Dietary protein intake and the progressive nature of kidney disease: The role of haemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation and intrinsic renal disease. N EnglJ Med 1982; 307: 652-59. 3. Zucchelli P, Cagnoli L, Casanova S, Donini U, Pasquali S. Focal glomerulosclerosisin patients with unilateral nephrectomy. Kidney Int 1983; 24: 649-55. 4. Mathillas O, Attman PO, Aurell M, Blohmé I, Brynger H, Granerus G, Westberg G. Long-term outcome of renal function and proteinuria in kidney transplant donors Proc ED TA-ERA 1984; 21: 574-78. 5. Tapson JS, Marshall SM, Tisdall SR, Wilkinson R, Ward MK, Kerr DNS. Renal function and blood pressure after donor nephrectomy Proc EDTA-ERA 1984, 21: 580-87. 6. Hoitsma AJ, Paul LC, Van Es LA, Koene RAP. Long-term follow-up of living kidney donors. Neth J Med 1985; 28: 226-30. 7. Anderson CF, Velosa JA, Frohnert PP, et al. The risks of unilateral nephrectomy Status of kidney donors 10-20 years postoperatively. Mayo Clin Proc 1985; 60: 367-74.