Case Report Management of Intraocular Hypertension During Hemodialysis by Intravenous Glucose Administration Turgay Saritas, MD,1 Antonis Koutsonas, MD,2 Peter Walter, MD,2 Ju¨rgen Floege, MD,1 and Thilo Kru¨ger, MD1 A 64-year-old woman with end-stage renal disease and retinopathy secondary to type 2 diabetes mellitus presented with recurrent episodes of left ocular pain and acute loss of visual acuity during hemodialysis. During these episodes, markedly elevated intraocular pressures were measured. Several local and systemic antiglaucoma drugs were administered without improvement of intraocular pressure, resulting in the necessity of a glaucoma drainage device (Ahmed valve). Due to a local infection, it had to be removed, after which intraocular pressure elevations recurred during hemodialysis. Assuming that intraocular changes in osmolality during hemodialysis caused the intraocular pressure increases, intradialytic administration of a 20% glucose solution (100 mL/h) was initiated. This completely abrogated the development of both intraocular pain and increases in intraocular pressure. Am J Kidney Dis. 63(3):500-502. ª 2014 by the National Kidney Foundation, Inc. INDEX WORDS: Hemodialysis; eye; intraocular pressure; blood glucose; diabetes mellitus.
O
cular complications are common in patients with end-stage renal disease treated with hemodialysis (HD).1 Fluctuations in intraocular pressure during or after HD have been documented in the literature, but are still diagnosed infrequently. Besides headache and nausea, intraocular hypertension can lead to long-term optic nerve damage and persistent amaurosis if not treated adequately.2 We describe a patient who developed recurrent symptomatic elevated intraocular pressure during HD; several antiglaucoma drugs and an implanted drainage device failed to control intraocular pressure. Finally, intravenous administration of a 20% hyperosmotic glucose solution managed symptomatic intradialytic intraocular pressure elevations.
CASE REPORT A 64-year-old woman with end-stage renal disease secondary to type 2 diabetes mellitus presented with recurrent episodes of severe left-sided ocular pain and visual disturbances ranging from blurred vision to loss of vision during HD. She had been on HD therapy since early 2010. Her medical history included complications of diabetes mellitus, including nephropathy, neuropathy, coronary heart disease, peripheral vascular disease, and retinopathy with macular edema, requiring both repeated topical and surgical treatments, such as photocoagulation, bevacizumab
From the Departments of 1Nephrology and Clinical Immunology and 2Ophthalmology, RWTH Aachen University, Aachen, Germany. Received April 12, 2013. Accepted in revised form August 21, 2013. Originally published online November 4, 2013. Address correspondence to Turgay Saritas, MD, Department of Nephrology and Clinical Immunology, RWTH Aachen University, Pauwelsstrasse 30, D-52074 Aachen, Germany. E-mail: tsaritas@ ukaachen.de 2014 by the National Kidney Foundation, Inc. 0272-6386/$36.00 http://dx.doi.org/10.1053/j.ajkd.2013.08.034 500
injection, and vitrectomy of both eyes. Nevertheless, she lost vision in the right eye and her unaided visual acuity in her left eye was 2/10. The best corrected visual acuity of the patient fluctuated between 20/200 and 20/100 (logMAR [magnification requirement] of 1.0-0.70), decreasing during painful episodes to hand motion. Near the end of 2010, an Ahmed valve was implanted. She also had chronic obstructive pulmonary disease and pulmonary hypertension after a smoking history of more than 80 pack-years. Medications include antihypertensive drugs, long-acting insulin (insulin glargin), and the usual drugs in terminal kidney failure. Since the start of HD therapy, intraocular pressure in the left eye was documented repeatedly by slit-lamp–mounted Goldmann applanation tonometry to increase to levels .30 mm Hg despite the regular use of a topical a-agonist (brimonidine twice daily), prostaglandin analogue (travoprost once daily), and carbonic anhydrase inhibitor with b-antagonist (brinzolamide with timolol twice daily). Several severe episodes (intraocular pressure up to 58 mm Hg) required anterior chamber paracentesis for emergency relief of the pain. Intraocular pressure was controlled temporarily after the Ahmed glaucoma valve implantation. However, due to endophthalmitis and dislocation of the Ahmed valve, its removal became necessary. Thereafter, intraocular pressure started to increase again during hemodialysis sessions. HD was performed routinely 3 times weekly for 5 hours using high-flux polysulfone dialyzers and bicarbonate dialysate (Fresenius Medical Care Germany). Dialysate composition was as follows: sodium, 140 mEq/L; potassium, 3 mEq/L; calcium, 1.25 mEq/L; glucose, 99.1 mg/dL; and bicarbonate, 32 mEq/L. A blood flow rate of 300 mL/min and average ultrafiltration flow rate of 355 mL/min were used. Mean blood glucose levels in our patient decreased not significantly during HD (mean of 12 HD sessions: before HD, 184 mg/dL; after 2 hours, 174 mg/dL; and 1 hour after HD, 172 mg/dL). After the prior ocular treatment strategies failed, we administered intravenous glucose (20% glucose at a rate of 100 mL/h) with each dialysis session to prevent the elevation in intraocular pressure during HD. During this treatment, mean blood glucose levels significantly increased (mean of 12 HD sessions: before HD, 189 mg/dL; after 2 hours, 288 mg/dL; and 1 hour after HD, 210 mg/dL). After this change in treatment, the patient no longer experienced episodes of ocular pain and ophthalmologic pharmacotherapy was tapered. Intraocular pressures measured after glucose-supplemented
Am J Kidney Dis. 2014;63(3):500-502
Glucose Administration Managed Intraocular Hypertension during Hemodialysis HD remained within normal ranges (Fig 1). With the use of glucose during HD, serum osmolality declined from w300 to 290 mOsm/kg at the end of dialysis. Eleven weeks after starting glucose therapy, hemoglobin A1c serum levels increased to a maximum of 8.0%. Nevertheless, hemoglobin A1c levels returned within 8 weeks to levels before glucose therapy (7.4%) and have remained without the dose of insulin needing to be adjusted (not shown).
DISCUSSION We report the successful treatment of increased intraocular pressures by administration of intravenous glucose during HD. Normal intraocular pressure ranges from 10-21 mm Hg. In HD patients without prior ocular disease, increased intraocular pressure during HD is unusual.3 In patients with ocular diseases in their history, such as glaucoma or eye-outflow obstruction, acute increases in intraocular pressure are much more common.4 As published recently, mean intraocular pressure significantly decreased after HD in nondiabetic patients, but not in diabetic patients.5 The relationship between diabetes and intraocular hypertension is not well established and has been discussed controversially for years. It is suggested that patients with diabetes mellitus are more likely to develop glaucoma than patients without diabetes mellitus.6
Figure 1. Time course of intraocular pressure (IOP; in millimeters of mercury) of the patient’s left eye in her history. Periods are indicated as follows: (A) 1: IOP before starting hemodialysis (HD) therapy; 2: first IOP elevations occur during HD; 3: IOP after implantation of Ahmed valve; (B) 4: after Ahmed valve explantation, IOP elevations during HD recurred; and 5: IOP when 20% glucose solution was administered at 100 mL/h during HD. Am J Kidney Dis. 2014;63(3):500-502
Since the first study by Sitprija et al7 in 1964, various theories have been put forth to explain the relationship between intraocular pressure changes and HD. During HD, osmotically active substances are removed, possibly more rapidly in plasma than in the eyes, causing an osmotic gap between both compartments.8-11 It has been suggested that the gap between cellular and serum urea levels during HD could be responsible for intraocular hypertension,12 although membranes are highly permeable for urea. Therefore, it has been proposed that due to the osmotic disequilibrium, shifting of water from plasma into the eye’s aqueous humor leads to intraocular pressure elevations.11 The decreased serum osmolality in our patient at the end of HD compared to that at the beginning of HD is consistent with this hypothesis. The uncommon occurrence of increased intraocular pressure in the general HD population might be explained by the mentioned lower risk in patients without previous ocular problems.3 Several therapeutic recommendations have been made to prevent a symptomatic increase in intraocular pressure during HD. In mild cases, topical eye solutions containing the b-antagonist timolol can stabilize intraocular pressure during HD.13 Additional use of a carbonic anhydrase inhibitor has been proved to effectively control intraocular pressure during HD.14 Nevertheless, carbonic anhydrase inhibitors can cause serious metabolic acidosis in patients with end-stage renal disease, and its use is discouraged in HD patients. More invasive approaches include trabeculoplasty and Ahmed valve implantation.11 The latter was performed successfully in our patient, although the implant had to be removed later due to local infection. Similar published cases described that the application of oral hypertonic glycerol,14 intravenous mannitol,15 or hypertonic sodium dialysis11 was able to control intraocular pressure. Nevertheless, these agents must be used with caution or are even contraindicated in patients on HD therapy. Mannitol is excreted mainly by the kidneys and is regarded to have an increased half-life up to 36 hours in HD patients, thus predisposing the patient to unwanted side effects.16 Hypertonic sodium solution may lead to thirst and can increase the interdialytic volume overload, leading to risks in subsequent increased fluid removal during dialysis. Increasing the dialysate sodium concentration by .10 mEq/L compared to serum sodium level is contraindicated, and stabilization of serum osmolality may not be achievable by lower dialysate/serum sodium concentration differences. In addition, higher dialysate sodium concentrations may cause higher blood pressures. Other modes of dialysis, such as peritoneal dialysis16 or slower urea removal,11 have 501
Saritas et al
been shown to decrease the risk of intraocular hypertension. One limitation of high glucose administration during dialysis is the increase in serum blood glucose levels, especially in diabetic patients. In our patient, we noted an increase in serum hemoglobin A1c levels to 8.0%, which returned to levels before glucose therapy (7.4%) without increasing antidiabetic therapy. Careful monitoring of intradialytic blood glucose levels is indicated in patients receiving this treatment. To our knowledge, we report the first case in which simple intravenous glucose administration successfully managed intraocular pressure elevations and serum hypo-osmolality during HD. We speculate that the increase in intraocular pressure is caused by a net influx of water into the eye due to a relative serum hypo-osmolality occurring during HD that can be prevented by concomitant glucose administration. Compared with alternative approaches that have been used in such cases, our strategy appears simple and safe.
ACKNOWLEDGEMENTS Support: None. Financial Disclosure: The authors declare that they have no relevant financial interests.
REFERENCES 1. Evans RD, Rosner M. Ocular abnormalities associated with advanced kidney disease and hemodialysis. Semin Dial. 2005;18: 252-257. 2. Weinreb RN, Khaw PT. Primary open-angle glaucoma. Lancet. 2004;363:1711-1720. 3. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120(6): 714-720; discussion 829-830.
502
4. Masuda H, Shibuza Y, Ohira A. Markedly increased unilateral intraocular pressure during hemodialysis in a patient with ipsilateral exfoliative glaucoma. Am J Ophthalmol. 2002;129: 534-536. 5. Afshar R, Ghasemi H, Shabpiray H, et al. Monitoring of intraocular pressure and its correlation with systemic parameters before and after hemodialysis. Iran J Kidney Dis. 2013;7(1):53-59. 6. Primus S, Harris A, Siesky BA, Guidoboni G. Diabetes: a risk factor for glaucoma? Br J Ophthalmol. 2011;95:1621-1622. 7. Sitprija V, Holmes JH, Ellis PP. Changes in intraocular pressure during hemodialysis. Invest Ophthalmol. 1964;3: 273-284. 8. Broekema N, Van Bijsterveld OP, De BosKuil RJC. Intraocular pressure during hemodialysis. Ophthalmologica. 1988;197: 60-64. 9. Samsudin A, Mimiwati Z, Soong T, Fauzi MS, Zabri K. Effect of haemodialysis on intraocular pressure. Eye (Lond). 2010;24:70-73. 10. Dinc UA, Ozdek S, Aktas Z, Guz G, Onol M. Changes in intraocular pressure, and corneal and retinal nerve fiber layer thickness during hemodialysis. Int Ophthalmol. 2010;30:337-340. 11. Tawara A, Kobata H, Fujisawa K, Abe T, Ohnishi Y. Mechanism of intraocular pressure elevation during hemodialysis. Curr Eye Res. 1998;17:339-347. 12. Tovbin D, Belfair N, Shapira S, et al. High postdialysis urea rebound can predict intradialytic increase in intraocular pressure in dialysis patients with lowered intradialytic hemoconcentration. Nephron. 2002;90:181-187. 13. Choong YF, Menage MJ. Symptomatic acute raised IOP following hemodialysis in a patient with end stage renal failure. Br J Ophthalmol. 1998;82:1342-1350. 14. Jaeger P, Morisod L, Wauters JP, Faggioni R. Prevention of glaucoma during hemodialysis by mannitol and acetazolamide. N Engl J Med. 1980;18:702. 15. Borges HF, Hocks J, Kjellstrand CM. Mannitol intoxication in patients with renal failure. Arch Intern Med. 1982;142(1):63-66. 16. De Marchi S, Cechin E, Tesio F. Intraocular pressure changes during hemodialysis: prevention of excessive dialytic rise and development of severe metabolic acidosis following acetazolamide therapy. Ren Fail. 1989;11:117-124.
Am J Kidney Dis. 2014;63(3):500-502
O
cular complications are common in patients with end-stage renal disease treated with hemodialysis (HD).1 Fluctuations in intraocular pressure during or after HD have been documented in the literature, but are still diagnosed infrequently. Besides headache and nausea, intraocular hypertension can lead to long-term optic nerve damage and persistent amaurosis if not treated adequately.2 We describe a patient who developed recurrent symptomatic elevated intraocular pressure during HD; several antiglaucoma drugs and an implanted drainage device failed to control intraocular pressure. Finally, intravenous administration of a 20% hyperosmotic glucose solution managed symptomatic intradialytic intraocular pressure elevations.
CASE REPORT A 64-year-old woman with end-stage renal disease secondary to type 2 diabetes mellitus presented with recurrent episodes of severe left-sided ocular pain and visual disturbances ranging from blurred vision to loss of vision during HD. She had been on HD therapy since early 2010. Her medical history included complications of diabetes mellitus, including nephropathy, neuropathy, coronary heart disease, peripheral vascular disease, and retinopathy with macular edema, requiring both repeated topical and surgical treatments, such as photocoagulation, bevacizumab
From the Departments of 1Nephrology and Clinical Immunology and 2Ophthalmology, RWTH Aachen University, Aachen, Germany. Received April 12, 2013. Accepted in revised form August 21, 2013. Originally published online November 4, 2013. Address correspondence to Turgay Saritas, MD, Department of Nephrology and Clinical Immunology, RWTH Aachen University, Pauwelsstrasse 30, D-52074 Aachen, Germany. E-mail: tsaritas@ ukaachen.de 2014 by the National Kidney Foundation, Inc. 0272-6386/$36.00 http://dx.doi.org/10.1053/j.ajkd.2013.08.034 500
injection, and vitrectomy of both eyes. Nevertheless, she lost vision in the right eye and her unaided visual acuity in her left eye was 2/10. The best corrected visual acuity of the patient fluctuated between 20/200 and 20/100 (logMAR [magnification requirement] of 1.0-0.70), decreasing during painful episodes to hand motion. Near the end of 2010, an Ahmed valve was implanted. She also had chronic obstructive pulmonary disease and pulmonary hypertension after a smoking history of more than 80 pack-years. Medications include antihypertensive drugs, long-acting insulin (insulin glargin), and the usual drugs in terminal kidney failure. Since the start of HD therapy, intraocular pressure in the left eye was documented repeatedly by slit-lamp–mounted Goldmann applanation tonometry to increase to levels .30 mm Hg despite the regular use of a topical a-agonist (brimonidine twice daily), prostaglandin analogue (travoprost once daily), and carbonic anhydrase inhibitor with b-antagonist (brinzolamide with timolol twice daily). Several severe episodes (intraocular pressure up to 58 mm Hg) required anterior chamber paracentesis for emergency relief of the pain. Intraocular pressure was controlled temporarily after the Ahmed glaucoma valve implantation. However, due to endophthalmitis and dislocation of the Ahmed valve, its removal became necessary. Thereafter, intraocular pressure started to increase again during hemodialysis sessions. HD was performed routinely 3 times weekly for 5 hours using high-flux polysulfone dialyzers and bicarbonate dialysate (Fresenius Medical Care Germany). Dialysate composition was as follows: sodium, 140 mEq/L; potassium, 3 mEq/L; calcium, 1.25 mEq/L; glucose, 99.1 mg/dL; and bicarbonate, 32 mEq/L. A blood flow rate of 300 mL/min and average ultrafiltration flow rate of 355 mL/min were used. Mean blood glucose levels in our patient decreased not significantly during HD (mean of 12 HD sessions: before HD, 184 mg/dL; after 2 hours, 174 mg/dL; and 1 hour after HD, 172 mg/dL). After the prior ocular treatment strategies failed, we administered intravenous glucose (20% glucose at a rate of 100 mL/h) with each dialysis session to prevent the elevation in intraocular pressure during HD. During this treatment, mean blood glucose levels significantly increased (mean of 12 HD sessions: before HD, 189 mg/dL; after 2 hours, 288 mg/dL; and 1 hour after HD, 210 mg/dL). After this change in treatment, the patient no longer experienced episodes of ocular pain and ophthalmologic pharmacotherapy was tapered. Intraocular pressures measured after glucose-supplemented
Am J Kidney Dis. 2014;63(3):500-502
Glucose Administration Managed Intraocular Hypertension during Hemodialysis HD remained within normal ranges (Fig 1). With the use of glucose during HD, serum osmolality declined from w300 to 290 mOsm/kg at the end of dialysis. Eleven weeks after starting glucose therapy, hemoglobin A1c serum levels increased to a maximum of 8.0%. Nevertheless, hemoglobin A1c levels returned within 8 weeks to levels before glucose therapy (7.4%) and have remained without the dose of insulin needing to be adjusted (not shown).
DISCUSSION We report the successful treatment of increased intraocular pressures by administration of intravenous glucose during HD. Normal intraocular pressure ranges from 10-21 mm Hg. In HD patients without prior ocular disease, increased intraocular pressure during HD is unusual.3 In patients with ocular diseases in their history, such as glaucoma or eye-outflow obstruction, acute increases in intraocular pressure are much more common.4 As published recently, mean intraocular pressure significantly decreased after HD in nondiabetic patients, but not in diabetic patients.5 The relationship between diabetes and intraocular hypertension is not well established and has been discussed controversially for years. It is suggested that patients with diabetes mellitus are more likely to develop glaucoma than patients without diabetes mellitus.6
Figure 1. Time course of intraocular pressure (IOP; in millimeters of mercury) of the patient’s left eye in her history. Periods are indicated as follows: (A) 1: IOP before starting hemodialysis (HD) therapy; 2: first IOP elevations occur during HD; 3: IOP after implantation of Ahmed valve; (B) 4: after Ahmed valve explantation, IOP elevations during HD recurred; and 5: IOP when 20% glucose solution was administered at 100 mL/h during HD. Am J Kidney Dis. 2014;63(3):500-502
Since the first study by Sitprija et al7 in 1964, various theories have been put forth to explain the relationship between intraocular pressure changes and HD. During HD, osmotically active substances are removed, possibly more rapidly in plasma than in the eyes, causing an osmotic gap between both compartments.8-11 It has been suggested that the gap between cellular and serum urea levels during HD could be responsible for intraocular hypertension,12 although membranes are highly permeable for urea. Therefore, it has been proposed that due to the osmotic disequilibrium, shifting of water from plasma into the eye’s aqueous humor leads to intraocular pressure elevations.11 The decreased serum osmolality in our patient at the end of HD compared to that at the beginning of HD is consistent with this hypothesis. The uncommon occurrence of increased intraocular pressure in the general HD population might be explained by the mentioned lower risk in patients without previous ocular problems.3 Several therapeutic recommendations have been made to prevent a symptomatic increase in intraocular pressure during HD. In mild cases, topical eye solutions containing the b-antagonist timolol can stabilize intraocular pressure during HD.13 Additional use of a carbonic anhydrase inhibitor has been proved to effectively control intraocular pressure during HD.14 Nevertheless, carbonic anhydrase inhibitors can cause serious metabolic acidosis in patients with end-stage renal disease, and its use is discouraged in HD patients. More invasive approaches include trabeculoplasty and Ahmed valve implantation.11 The latter was performed successfully in our patient, although the implant had to be removed later due to local infection. Similar published cases described that the application of oral hypertonic glycerol,14 intravenous mannitol,15 or hypertonic sodium dialysis11 was able to control intraocular pressure. Nevertheless, these agents must be used with caution or are even contraindicated in patients on HD therapy. Mannitol is excreted mainly by the kidneys and is regarded to have an increased half-life up to 36 hours in HD patients, thus predisposing the patient to unwanted side effects.16 Hypertonic sodium solution may lead to thirst and can increase the interdialytic volume overload, leading to risks in subsequent increased fluid removal during dialysis. Increasing the dialysate sodium concentration by .10 mEq/L compared to serum sodium level is contraindicated, and stabilization of serum osmolality may not be achievable by lower dialysate/serum sodium concentration differences. In addition, higher dialysate sodium concentrations may cause higher blood pressures. Other modes of dialysis, such as peritoneal dialysis16 or slower urea removal,11 have 501
Saritas et al
been shown to decrease the risk of intraocular hypertension. One limitation of high glucose administration during dialysis is the increase in serum blood glucose levels, especially in diabetic patients. In our patient, we noted an increase in serum hemoglobin A1c levels to 8.0%, which returned to levels before glucose therapy (7.4%) without increasing antidiabetic therapy. Careful monitoring of intradialytic blood glucose levels is indicated in patients receiving this treatment. To our knowledge, we report the first case in which simple intravenous glucose administration successfully managed intraocular pressure elevations and serum hypo-osmolality during HD. We speculate that the increase in intraocular pressure is caused by a net influx of water into the eye due to a relative serum hypo-osmolality occurring during HD that can be prevented by concomitant glucose administration. Compared with alternative approaches that have been used in such cases, our strategy appears simple and safe.
ACKNOWLEDGEMENTS Support: None. Financial Disclosure: The authors declare that they have no relevant financial interests.
REFERENCES 1. Evans RD, Rosner M. Ocular abnormalities associated with advanced kidney disease and hemodialysis. Semin Dial. 2005;18: 252-257. 2. Weinreb RN, Khaw PT. Primary open-angle glaucoma. Lancet. 2004;363:1711-1720. 3. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120(6): 714-720; discussion 829-830.
502
4. Masuda H, Shibuza Y, Ohira A. Markedly increased unilateral intraocular pressure during hemodialysis in a patient with ipsilateral exfoliative glaucoma. Am J Ophthalmol. 2002;129: 534-536. 5. Afshar R, Ghasemi H, Shabpiray H, et al. Monitoring of intraocular pressure and its correlation with systemic parameters before and after hemodialysis. Iran J Kidney Dis. 2013;7(1):53-59. 6. Primus S, Harris A, Siesky BA, Guidoboni G. Diabetes: a risk factor for glaucoma? Br J Ophthalmol. 2011;95:1621-1622. 7. Sitprija V, Holmes JH, Ellis PP. Changes in intraocular pressure during hemodialysis. Invest Ophthalmol. 1964;3: 273-284. 8. Broekema N, Van Bijsterveld OP, De BosKuil RJC. Intraocular pressure during hemodialysis. Ophthalmologica. 1988;197: 60-64. 9. Samsudin A, Mimiwati Z, Soong T, Fauzi MS, Zabri K. Effect of haemodialysis on intraocular pressure. Eye (Lond). 2010;24:70-73. 10. Dinc UA, Ozdek S, Aktas Z, Guz G, Onol M. Changes in intraocular pressure, and corneal and retinal nerve fiber layer thickness during hemodialysis. Int Ophthalmol. 2010;30:337-340. 11. Tawara A, Kobata H, Fujisawa K, Abe T, Ohnishi Y. Mechanism of intraocular pressure elevation during hemodialysis. Curr Eye Res. 1998;17:339-347. 12. Tovbin D, Belfair N, Shapira S, et al. High postdialysis urea rebound can predict intradialytic increase in intraocular pressure in dialysis patients with lowered intradialytic hemoconcentration. Nephron. 2002;90:181-187. 13. Choong YF, Menage MJ. Symptomatic acute raised IOP following hemodialysis in a patient with end stage renal failure. Br J Ophthalmol. 1998;82:1342-1350. 14. Jaeger P, Morisod L, Wauters JP, Faggioni R. Prevention of glaucoma during hemodialysis by mannitol and acetazolamide. N Engl J Med. 1980;18:702. 15. Borges HF, Hocks J, Kjellstrand CM. Mannitol intoxication in patients with renal failure. Arch Intern Med. 1982;142(1):63-66. 16. De Marchi S, Cechin E, Tesio F. Intraocular pressure changes during hemodialysis: prevention of excessive dialytic rise and development of severe metabolic acidosis following acetazolamide therapy. Ren Fail. 1989;11:117-124.
Am J Kidney Dis. 2014;63(3):500-502
