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Medical Associates  ·  Department of Nephrology ← Maintenance Hemodialysis  ·  urinenephrology.org
Clinical Mastery Series  ·  Maintenance Hemodialysis

Intradialytic hypertension and the stability trade-off

Defining the pre-to-post rise, what drives it, and why buying hemodynamic stability with chronic blood pressure is usually a bad trade.
Andrew Bland, MD, FACP, FAAP UICOMP · UDPA · Butler COM Reviewed September 2026 13 min read

Part of the Maintenance Hemodialysis mastery module. Reviewed September 2026.

Bottom line

  • Define it by pattern, not by one session. KDIGO 2020: a systolic rise of more than 10 mmHg from pre- to post-dialysis into the hypertensive range in at least 4 of 6 consecutive treatments should prompt fuller evaluation, including out-of-unit BP and a critical look at dry weight 1.
  • It is a prognostic signal. Persistent intradialytic hypertension (IDHTN) is reported in 15–30% of patients and carries a two- to four-fold increased risk of hospitalization, all-cause mortality, and cardiovascular mortality; whether that is causal is unresolved 2,3.
  • Look for the mechanism. Subclinical volume overload, sodium gain from dialysate above plasma sodium, high-calcium dialysate, ESA dosing, and removal of dialyzable antihypertensives mid-session are all candidates 1,2.
  • Do not buy hemodynamic stability with chronic BP as a strategy. Raising dialysate sodium from 135 to 140 mEq/L cut the odds of intradialytic hypotension (IDH) by one-third (OR 0.66) but added 7.0/3.9 mmHg of pre-dialysis BP in a small within-patient extension phase 4 — and both sides of that trade are associated with death 2,5.
  • Buy stability with time, sodium restriction, frequency, drug selection, and individualized cooling instead. Centre-wide cooling did not improve cardiovascular outcomes in MyTEMP (HR 1.00) 6, and RESOLVE, the trial of default dialysate sodium, has not reported 7.

1. The targets this page assumes

Out-of-unit BP is the treatment target: home BP below 135/85 mmHg or ambulatory BP below 130/80 mmHg 8,9. For units that still steer by non-standardized in-centre readings, the UK Kidney Association 2025 guideline sets a safety envelope of pre-dialysis systolic 140–165 mmHg (grade 2B) and post-dialysis systolic 120–140 mmHg (2C) 9. Those numbers bound what follows. Measurement itself is covered in Which blood pressure matters, and drug treatment in Treating hypertension on dialysis.

2. Definition, frequency, and prognosis

A single post-dialysis reading higher than the pre-dialysis reading is common and means little. What matters is a reproducible pattern. KDIGO 2020 defines the actionable pattern as a systolic rise of more than 10 mmHg from pre- to post-dialysis into the hypertensive range in at least 4 of 6 consecutive treatments, which excludes sporadic events 1.

QuestionWhat the evidence shows
How common?Prevalence runs 5–15% depending on definition 1; persistent IDHTN (>10 mmHg rise) is reported in 15–30% of patients 2
Does it matter?Two- to four-fold increased risk of hospitalization, all-cause mortality, and cardiovascular mortality 2 (observational)
Causal or marker?Unresolved. Patients with IDHTN are older, with lower albumin, lower Kt/V, and more antihypertensive use, which suggests vascular stiffness and comorbidity burden may carry some of the risk; the association is consistent across cohorts 2,3

The practical consequence of “unresolved” is that the pattern earns an evaluation, not a reflex. The evaluation starts with out-of-unit BP and a critical look at dry weight 1, because chronic subclinical volume overload is the first mechanism on the list 1,2.

3. Mechanism: what to look for

The review lists the proposed mechanisms of IDHTN 1,2:

  • chronic subclinical volume overload with the lag phenomenon;
  • intradialytic sympathetic and renin–angiotensin activation;
  • endothelin-1 release with impaired nitric oxide bioavailability;
  • intradialytic sodium gain when dialysate sodium exceeds plasma sodium;
  • high-calcium dialysate;
  • ESA administration; and
  • removal of dialyzable antihypertensive agents mid-session.

Three of these map directly onto decisions already in the chart: whether the target weight is right (volume overload, tested with out-of-unit BP and objective volume assessment 1), whether the dialysate sodium exceeds the patient’s plasma sodium, and whether the patient takes a dialyzable antihypertensive before treatment 1,2.

The last mechanism is the direct link to drug timing: a patient whose BP climbs during dialysis may simply be dialyzing off their atenolol or lisinopril 1,2. Agent selection and dose timing are covered in Treating hypertension on dialysis.

Volume is not the whole story, and the two bioimpedance studies disagree. One found IDHTN equally common across low, normal, and high volume states 2; another, in 531 patients, found more post-dialysis extracellular overhydration in patients whose systolic BP rose 10. The reasonable reading is that volume excess is a common cause of the pattern but not a safe assumption in any individual patient.

4. The work-up the pattern earns

KDIGO 2020 asks for “fuller evaluation, including out-of-unit BP and a critical look at dry weight” once the 4-of-6 pattern is established 1. Translated into steps that the rest of the evidence supports:

  1. Get an out-of-unit BP. One week of duplicate morning and evening home readings on a validated upper-arm device, including at least one non-dialysis day, detects ambulatory hypertension better than two weeks of pre-dialysis readings (AUC 0.934 versus 0.778) 11. KDIGO 2020 also accepts twice-daily readings for 4 days after the midweek treatment 1. A home average of 135/85 mmHg or higher is hypertension 8.
  2. Look objectively for volume excess. Crackles and edema share only 12% and 4% of their variance with ultrasound-detected lung water 12. Lung ultrasound finds congestion the examination misses, although a lung-ultrasound-guided strategy did not significantly improve hard outcomes in LUST (HR 0.88; 0.63–1.24) 13; flat relative plasma volume slopes indicate expansion 14.
  3. If volume is the hypothesis, test it over weeks. In DRIP (randomized), probing added 0.1 kg per 10 kg body weight per session, halved the step when it was not tolerated, and lowered ambulatory systolic BP by approximately 7 mmHg by 4 weeks 15. Judge the result by home BP or ABPM, not by the next pre-dialysis reading.
  4. Keep the rate ceiling. If the target weight cannot be reached below 13 mL/kg/h, add time rather than rate; ultrafiltration rates above that threshold are associated with higher all-cause and cardiovascular mortality 16,17.
  5. Check the drug list and the dialysate. A dialyzable agent taken before treatment may be dialyzed off mid-session 1,2; if a drug is implicated in IDH, UKKA prefers consistent evening dosing over omission (2D) 9. Dialysate sodium above plasma sodium is a source of intradialytic sodium gain 1,2.

5. Do you tolerate post-dialysis hypertension to mitigate IDH?

The question arises because the two hemodynamic problems pull in opposite directions. The levers that protect against intradialytic hypotension (leaving fluid on, raising dialysate sodium, holding ultrafiltration) tend to leave the patient hypertensive after the treatment and between treatments. The answer: no as a strategy, sometimes yes as a tactic in an individual patient, and never without a plan to exit.

5.1 What intradialytic hypotension costs

The other side of the trade is not trivial. By EBPG criteria or a nadir systolic BP below 90 mmHg, IDH complicates approximately 10–12% of sessions (10.1% and 11.6% in pooled analyses) 18. Nadir-based definitions carry the strongest mortality signal: a nadir below 90 mmHg in at least 30% of sessions was associated with higher mortality (adjusted HR 1.38 in HEMO; 1.22 in a large dialysis organization cohort), with or without symptoms, and about 10–12% of patients meet that threshold 5. IDH is associated with access thrombosis, inadequate delivered dose, cardiovascular events, and death 1,5,19. Intradialytic hypotension itself is covered in Intradialytic hypotension and dialysate cooling.

5.2 The trade is real and measurable

Miskulin and colleagues randomized 42 patients 2:1 to dialysate sodium 135 versus 138 mEq/L for 6 months, then, in a non-randomized 12-week extension, raised the 135 arm to 140 mEq/L within patients 4:

Effect of raising dialysate sodium 135 → 140 mEq/L (extension phase, within-patient)Magnitude
Intradialytic hypotensionOR 0.66 (0.45–0.97): reduced
Pre-dialysis BP+7.0 (4.8–9.2) / +3.9 (2.6–5.1) mmHg
Interdialytic weight gain+0.2 (0.1–0.3) kg

That is the exchange rate, measured in a small within-patient comparison. In the randomized phase, 135 versus 138 mEq/L produced no difference in IDH and no difference in pre-dialysis BP, a small reduction in interdialytic weight gain, and more symptoms 4. Pooled across 17 mostly short, small trials, low dialysate sodium reduced weight gain and probably BP, but probably increased IDH (RR 1.58) and cramps (RR 1.84), with no data on death or cardiovascular events 20. The sodium lever is asymmetric in practice.

The trial that could settle the default, RESOLVE, cluster-randomizes units to dialysate sodium 137 versus 140 mmol/L. As of September 2026 it has not reported: its registry lists it as recruiting, with estimated primary completion in December 2026 7. The full dialysate-sodium evidence is in Dialysate sodium: BP, thirst, IDH, and the RESOLVE question.

flowchart LR
    S["Goal: reduce<br>intradialytic hypotension"] --> P1["Path A: concede chronic BP<br>Raise dialysate sodium,<br>hold ultrafiltration,<br>accept post-HD hypertension"]
    S --> P2["Path B: change the<br>dialysis prescription<br>and drug selection"]
    P1 --> C1["IDH odds ratio 0.66"]
    P1 --> C2["Pre-dialysis BP plus 7.0 / 3.9 mmHg<br>Interdialytic weight gain plus 0.2 kg"]
    C2 --> C3["Post-dialytic BP rise is itself<br>a 2 to 4 fold mortality signal"]
    C3 --> C4["Higher starting weight next session,<br>higher UF requirement,<br>more IDH risk"]
    C4 --> S
    P2 --> B1["Longer or more frequent sessions<br>lower UF rate at same volume"]
    P2 --> B2["Cooler dialysate, individualized"]
    P2 --> B3["Swap a vasodilating beta blocker<br>such as carvedilol for a<br>cardioselective agent"]
    P2 --> B4["Sodium restriction<br>to reduce weight gain"]
    B1 --> G["Stability gained<br>without conceding<br>chronic blood pressure"]
    B2 --> G
    B3 --> G
    B4 --> G
    style S fill:#e7f5ff,stroke:#1971c2,color:#000
    style P1 fill:#ffe8cc,stroke:#e8590c,color:#000
    style P2 fill:#d0ebff,stroke:#1971c2,color:#000
    style C1 fill:#b2f2bb,stroke:#2f9e44,color:#000
    style C2 fill:#ffc9c9,stroke:#e03131,color:#000
    style C3 fill:#ffa8a8,stroke:#c92a2a,color:#000
    style C4 fill:#ff6b6b,stroke:#c92a2a,color:#fff
    style B1 fill:#d0ebff,stroke:#1971c2,color:#000
    style B2 fill:#d0ebff,stroke:#1971c2,color:#000
    style B3 fill:#d0ebff,stroke:#1971c2,color:#000
    style B4 fill:#d0ebff,stroke:#1971c2,color:#000
    style G fill:#b2f2bb,stroke:#2f9e44,color:#000
Figure 1. The Exchange Rate — What Buying Hemodynamic Stability Actually Costs. Path A buys a lower IDH risk with chronic BP and weight gain, and the higher starting weight feeds back into the next session. Path B changes time, temperature, drug selection, and sodium intake instead. Effect sizes are from the extension phase of a 42-patient trial 4; the 2–4-fold signal for post-dialytic BP rise is observational 2. Adapted from the canonical review.

5.3 Why the trade is usually bad

  • Both sides are mortality signals. A post-dialytic and intradialytic BP rise is an independent mortality signal 2,3, and so is frequent nadir-based IDH 5.
  • Higher post-dialysis BP often reflects incomplete volume removal, which drives interdialytic load, left ventricular hypertrophy, and pulmonary congestion 10,12,21.
  • The strategy is self-reinforcing in the wrong direction. Fluid left on today is a higher starting weight and a higher ultrafiltration requirement tomorrow, which raises the IDH risk the trade was meant to reduce.

5.4 Where a permissive post-dialysis BP is defensible

The defensible case is narrow: the elderly patient with autonomic failure, low ejection fraction or severe diastolic dysfunction, recurrent symptomatic nadirs below 90 mmHg despite optimized time and temperature, minimal interdialytic weight gain, and a weight near dry weight. Here you are treating a fixed cardiac-output limitation, not avoiding the work of volume management. Document the rationale, bound it at a post-dialysis systolic of 140 mmHg (the top of the UKKA 120–140 range) 9, and re-test every few months.

Warning — the exit plan

The condition is “never without a plan to exit.” The defensible version names the reason (autonomic failure or fixed low cardiac output), the ceiling (post-dialysis systolic 140 mmHg, the top of the UKKA range), and a re-test every few months 9.

6. Buying stability without spending chronic BP

Stability can be bought with interventions that do not cost chronic BP:

InterventionEvidence
Reduce the ultrafiltration rate below 10–13 mL/h/kg by lengthening time, not by leaving fluid onConsistent observational mortality data 16,17,22
Reduce interdialytic weight gain with sodium restriction (≤5 g salt/day)UKKA grade 1B; addresses the driver 9
More frequent or nocturnal dialysisRandomized evidence for left ventricular mass, BP, and antihypertensive burden 23,24
Cooler dialysate (35.5–36.0 °C)Reduces IDH and stunning in small studies. MyTEMP (cluster-randomized, 84 centers, 15,413 patients) found no cardiovascular outcome benefit from a centre-wide personalized-cooling policy (HR 1.00; 96% CI 0.89–1.11) and no meaningful difference in intradialytic systolic fall (26.6 versus 27.1 mmHg) 6. Reasonable as individualized therapy; not supported as blanket policy
Replace a vasodilating β-blocker (carvedilol) with a cardioselective agentAssimon 2018, observational 25; the dialyzability question itself is unresolved 1,9,26
Avoid food intake during dialysis; midodrine 2.5–10 mg before dialysis in refractory casesA systematic review of small, short studies supports hemodynamic efficacy 27; UKKA: may be considered (2C) 9; observational data associate midodrine use with higher mortality (adjusted IRR 1.37), almost certainly confounding by indication, and randomized outcome data are absent 28
Isolated ultrafiltration, UF profiling, blood-volume biofeedbackPhysiologically rational, weak outcome evidence; sodium profiling was associated with higher mortality in DOPPS 22

Rate and time are covered in Ultrafiltration rate and treatment time; cooling and the IDH response in Intradialytic hypotension and dialysate cooling.

Clinical Pearl — the carvedilol swap

In a hypertensive patient with frequent IDH and no heart failure with reduced ejection fraction, swapping carvedilol for a cardioselective agent is one of the few moves that can reduce IDH without conceding chronic BP 25. The exception runs the other way: in HFrEF or dilated cardiomyopathy, the only placebo-controlled survival trial of a β-blocker in dialysis used carvedilol, so keep it there and manage IDH around it 29.

7. Common questions

Should I lower dialysate sodium to control BP?

Not below about 138 mEq/L expecting benefit on current trial evidence. In the 42-patient randomized trial, 135 versus 138 mEq/L produced no difference in IDH or pre-dialysis BP, a small fall in weight gain, and more symptoms 4. Pooled trials show lower sodium reduces weight gain and probably BP but probably increases IDH (RR 1.58) and cramps 20. Raising sodium from 135 to 140 reduced IDH but cost approximately 7 mmHg of pre-dialysis systolic load 4. RESOLVE has not reported; as of 2026-09-26 its registry lists it as recruiting, with no results published or presented 7. Keep dialysate sodium at or just below plasma sodium.

Cool dialysate: yes or no?

Individualized yes, blanket policy no. MyTEMP, across 84 centers and 15,413 patients, found no cardiovascular benefit from a centre-wide personalized cooler-dialysate policy (HR 1.00) 6. Cooling remains reasonable for the specific IDH-prone patient.

Should patients hold BP medicines before dialysis to prevent IDH?

Not reflexively. Withholding is the same trade in pill form: a possible reduction in IDH bought with chronic BP. Nearly half of patients (46% of 189 surveyed) report withholding at least one antihypertensive before dialysis, most on physician advice 1,30. In TAKE-HOLD (cluster-randomized, 131 patients, 4 weeks), taking medications was not shown non-inferior to holding for asymptomatic IDH (difference 8%; 95% CI −3% to 19%) but was superior for uncontrolled pre-dialysis hypertension (difference −15%; −28% to −1%) 31. UKKA advises against routine omission and suggests consistent evening dosing for a drug implicated in IDH (2D) 9. Reserve withholding for documented nadir-based IDH, and apply it to the specific offending agent.

Is there ever a patient in whom I accept post-dialysis hypertension?

Yes: the elderly patient with autonomic failure or fixed low cardiac output, minimal weight gain, at dry weight, with recurrent symptomatic nadirs despite optimized time and temperature. Document it, bound it at a post-dialysis systolic of 140 mmHg 9, and revisit it every few months.

Evidence gaps

  • IDHTN has no outcome-based treatment trial. Whether the pattern causes harm or marks vascular stiffness and comorbidity remains unresolved 2,3.
  • Dialysate sodium: RESOLVE (cluster-randomized, default 137 versus 140 mmol/L) remains unreported as of September 2026, with estimated primary completion in December 2026 7. The Cochrane review found no trial reporting death or cardiovascular events 20.
  • IDH prevention has no intervention with proven mortality benefit, and MyTEMP eliminated the most popular candidate as a system-level policy 6.
  • Midodrine has hemodynamic data from small, short studies and no randomized outcome data 27,28.
  • β-blocker choice in the IDH-prone patient rests on conflicting observational analyses; no randomized comparison exists 25,26.

At the chair

Chair-side summary

Track the pattern across sessions. A systolic rise of more than 10 mmHg from pre- to post-dialysis into the hypertensive range in 4 of 6 consecutive treatments is a flag for review 1. Record the lowest intradialytic systolic BP every treatment, and treat a nadir below 90 mmHg as a reason to reassess even when the patient feels fine 1,5. The nursing card lists what to record and when to call.

Nursing card N6: Blood pressure at the chair →

References

Adapted from the author’s canonical review Blood Pressure in the Dialysis Patient (reference-checked 2026-09-26; every journal reference matched to its PubMed record). Numbering is local to this page.

  1. Flythe JE, Chang TI, Gallagher MP, et al; Conference Participants. Blood pressure and volume management in dialysis: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2020;97(5):861–876. PMID: 32278617
  2. Prasad B, Hemmett J, Suri R. Five things to know about intradialytic hypertension. Can J Kidney Health Dis. 2022;9:20543581221106657. PMID: 35756329
  3. Van Buren PN, Toto R, Inrig JK. Interdialytic ambulatory blood pressure in patients with intradialytic hypertension. Curr Opin Nephrol Hypertens. 2012;21(1):15–23. PMID: 22123207
  4. Miskulin DC, Tighiouart H, Hsu CM, Weiner DE. Dialysate sodium lowering in maintenance hemodialysis: a randomized clinical trial. Clin J Am Soc Nephrol. 2024;19(6):712–722. PMID: 38349776
  5. Flythe JE, Xue H, Lynch KE, Curhan GC, Brunelli SM. Association of mortality risk with various definitions of intradialytic hypotension. J Am Soc Nephrol. 2015;26(3):724–734. PMID: 25270068
  6. MyTEMP writing committee. Personalised cooler dialysate for patients receiving maintenance haemodialysis (MyTEMP): a pragmatic, cluster-randomised trial. Lancet. 2022;400(10364):1693–1703. PMID: 36343653
  7. Smyth B, Krishnasamy R, Jardine M; RESOLVE Study Global Team. Are observational reports on the association of dialysate sodium with mortality enough to change practice? Perspective from the RESOLVE Study Team. J Am Soc Nephrol. 2024;35(2):229–231. Trial registration NCT02823821 (registry status “Recruiting,” estimated primary completion December 2026; checked 2026-09-26). PMID: 38096088
  8. Sarafidis PA, Persu A, Agarwal R, et al. Hypertension in dialysis patients: a consensus document by the European Renal and Cardiovascular Medicine (EURECA-m) working group of the ERA-EDTA and the Hypertension and the Kidney working group of the ESH. Nephrol Dial Transplant. 2017;32(4):620–640. PMID: 28340239
  9. Doulton T, Adam M, Durman K, et al. Management of blood pressure in adults, children and young people on dialysis: UK Kidney Association clinical practice guideline. BMC Nephrol. 2025;26(1):532. PMID: 41013409
  10. Nongnuch A, Campbell N, Stern E, El-Kateb S, Fuentes L, Davenport A. Increased postdialysis systolic blood pressure is associated with extracellular overhydration in hemodialysis outpatients. Kidney Int. 2015;87(2):452–457. PMID: 25075771
  11. Leonidou K, Georgianos PI, Kollias A, et al. Home versus routine dialysis-unit blood pressure recordings among patients on hemodialysis. J Hum Hypertens. 2025;39(5):355–361. PMID: 40097627
  12. Torino C, Gargani L, Sicari R, et al. The agreement between auscultation and lung ultrasound in hemodialysis patients: the LUST study. Clin J Am Soc Nephrol. 2016;11(11):2005–2011. PMID: 27660305
  13. Zoccali C, Torino C, Mallamaci F, et al. A randomized multicenter trial on a lung ultrasound-guided treatment strategy in patients on chronic hemodialysis with high cardiovascular risk. Kidney Int. 2021;100(6):1325–1333. PMID: 34418415
  14. Sinha AD, Light RP, Agarwal R. Relative plasma volume monitoring during hemodialysis aids the assessment of dry weight. Hypertension. 2010;55(2):305–311. PMID: 20038754
  15. Agarwal R, Alborzi P, Satyan S, Light RP. Dry-weight reduction in hypertensive hemodialysis patients (DRIP): a randomized, controlled trial. Hypertension. 2009;53(3):500–507. PMID: 19153263
  16. Flythe JE, Kimmel SE, Brunelli SM. Rapid fluid removal during dialysis is associated with cardiovascular morbidity and mortality. Kidney Int. 2011;79(2):250–257. PMID: 20927040
  17. Assimon MM, Wenger JB, Wang L, Flythe JE. Ultrafiltration rate and mortality in maintenance hemodialysis patients. Am J Kidney Dis. 2016;68(6):911–922. PMID: 27575009
  18. Kuipers J, Verboom LM, Ipema KJR, et al. The prevalence of intradialytic hypotension in patients on conventional hemodialysis: a systematic review with meta-analysis. Am J Nephrol. 2019;49(6):497–506. PMID: 31129661
  19. Stefánsson BV, Brunelli SM, Cabrera C, et al. Intradialytic hypotension and risk of cardiovascular disease. Clin J Am Soc Nephrol. 2014;9(12):2124–2132. PMID: 25376764
  20. Marshall MR, Wang MY, Vandal AC, Dunlop JL. Low dialysate sodium levels for chronic haemodialysis. Cochrane Database Syst Rev. 2024;11(11):CD011204. PMID: 39498822
  21. Agarwal R. Hypervolemia is associated with increased mortality among hemodialysis patients. Hypertension. 2010;56(3):512–517. PMID: 20625076
  22. Dasgupta I, Thomas GN, Clarke J, et al. Associations between hemodialysis facility practices to manage fluid volume and intradialytic hypotension and patient outcomes. Clin J Am Soc Nephrol. 2019;14(3):385–393. PMID: 30723164
  23. FHN Trial Group; Chertow GM, Levin NW, Beck GJ, et al. In-center hemodialysis six times per week versus three times per week. N Engl J Med. 2010;363(24):2287–2300. PMID: 21091062
  24. Kotanko P, Garg AX, Depner T, et al. Effects of frequent hemodialysis on blood pressure: results from the randomized Frequent Hemodialysis Network trials. Hemodial Int. 2015;19(3):386–401. PMID: 25560227
  25. Assimon MM, Brookhart MA, Fine JP, Heiss G, Layton JB, Flythe JE. A comparative study of carvedilol versus metoprolol initiation and 1-year mortality among individuals receiving maintenance hemodialysis. Am J Kidney Dis. 2018;72(3):337–348. PMID: 29653770
  26. Weir MA, Dixon SN, Fleet JL, et al. β-Blocker dialyzability and mortality in older patients receiving hemodialysis. J Am Soc Nephrol. 2015;26(4):987–996. PMID: 25359874
  27. Prakash S, Garg AX, Heidenheim AP, House AA. Midodrine appears to be safe and effective for dialysis-induced hypotension: a systematic review. Nephrol Dial Transplant. 2004;19(10):2553–2558. PMID: 15280522
  28. Brunelli SM, Cohen DE, Marlowe G, Van Wyck D. The impact of midodrine on outcomes in patients with intradialytic hypotension. Am J Nephrol. 2018;48(5):381–388. PMID: 30423552
  29. Cice G, Ferrara L, D'Andrea A, et al. Carvedilol increases two-year survival in dialysis patients with dilated cardiomyopathy: a prospective, placebo-controlled trial. J Am Coll Cardiol. 2003;41(9):1438–1444. PMID: 12742278
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Also in this module

Blood pressure, volume, and the dialysis prescription, one question per page.