Prevalence, Associated Factors, and Prognosis of Acute Kidney Injury in Severe Malaria Among Sub-Saharan Africans

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Introduction

Globally, in 2023, the number of malaria cases was estimated at 263 million, with an incidence of 60.4 cases per 1000 population at risk [1]. This is an increase of 11 million cases from the previous year and a rise in incidence from 58.6 cases per 1000 population at risk in 2022 [1]. The world health organization (WHO) African Region continues to carry the heaviest burden of the disease, accounting for an estimated 94% of malaria cases worldwide in 2023. The WHO African Region continues to carry the heaviest burden of mortality, with 95% of estimated malaria deaths worldwide [1]. The severity of malaria is related to its possible visceral complications, particularly acute kidney injury (AKI). AKI is one of the most severe complications of severe malaria, with an overall incidence reaching 60% and a mortality rate of up to 45% [2]. AKI is a frequent life-threatening complication of severe malaria that can increase risk of death and long-term morbidity [3]. The aims of this study were to determine the prevalence of AKI during severe malaria, to describe the factors associated with the occurrence of AKI in patients with severe malaria, and to describe the impact of AKI on vital prognosis during severe malaria.

 

Patients and methods

This was a retrospective, descriptive, and analytical study conducted over a 5-year period from January 1, 2019 to December 31, 2023. The study was carried out in two nephrology departments (Dalal Jamm, and Ouakam military hospitals), three intensive care units (Dalal Jamm, Pikine, and Idrissa Pouye General hospitals), and an infectious diseases department (Fann hospital). Dalal Jamm, Pikine, Ouakam, Fann, and Idrissa Pouye General hospitals are publicly funded institution affiliated with the faculty of medicine of Cheikh Anta Diop University.

Study population

Patients with severe malaria were included. Patients with known End-Stage Renal Disease (ESRD) prior to the diagnosis of malaria were not included.

Study variables

Severe malaria was defined according to WHO criteria [4]. Severe falciparum malaria is defined as one or more of the manifestations described in Table 1, occurring in the absence of an identified alternative cause and in the presence of P. falciparum asexual parasitaemia. Severe vivax malaria is defined as for falciparum malaria but with no parasite density thresholds. Severe Plasmodium knowlesi malaria is defined according to the criteria used for Plasmodium falciparum malaria, with two specific exceptions: (1) P. knowlesi hyperparasitaemia defined as a parasite density > 100,000/μL; (2) presence of jaundice associated with a parasite density > 20,000/μL [4]. The diagnosis of AKI was based on the Kidney Disease Improving Global Outcomes (KDIGO) 2012 criteria [5]. Serum creatinine was measured in patients upon admission to hospital. For patients with a previous serum creatinine in the 7-365 days prior to admission, the most recent serum creatinine value was considered the baseline creatinine. For patients without a baseline creatinine in the 7-365 days prior to admission, the admission creatinine was imputed on the basis of a Modification of Diet in Renal Disease (MDRD) estimated glomerular filtration rate (eGFR) of 75 ml/min/1.73m² as per the KDIGO AKI guidelines [5]. Peak serum urea and serum creatinine levels were reported. Urine output was collected via Foley catheterization. Anuria and oliguria were defined, respectively, as urine output less than 300 mL/day and 500 mL/day. We used the SOFA excluding renal injury (non-renal SOFA) to assess the severity of the disease.

Criteria	Definition / Threshold
Impaired Consciousness	Glasgow Coma Score < 11 (adults) or Blantyre Coma Score < 3 (children)
Prostration	Generalized weakness: unable to sit, stand, or walk without assistance
Multiple Convulsions	More than 2 episodes within 24 hours
Acidosis	Base deficit > 8 mEq/L OR plasma bicarbonate < 15 mmol/L OR venous plasma lactate ≥ 5 mmol/L; manifests as respiratory distress (rapid, deep, labored breathing)
Hypoglycaemia	Blood/plasma glucose < 2.2 mmol/L (< 40 mg/dL)
Severe Malarial Anaemia	Children < 12 years: Hb ≤ 5 g/dL or hematocrit ≤ 15%; Adults: Hb < 7 g/dL or hematocrit < 20%; plus parasite count > 10,000/μL
Renal Impairment	Plasma/serum creatinine > 265 μmol/L (3 mg/dL) OR blood urea > 20 mmol/L
Jaundice	Plasma/serum bilirubin > 50 μmol/L (3 mg/dL) with parasite count > 100,000/μL
Pulmonary Oedema	Radiologically confirmed OR oxygen saturation < 92% on room air + respiratory rate > 30/min, often with chest indrawing and crepitations on auscultation
Significant Bleeding	Recurrent/prolonged bleeding (e.g., nose, gums, venepuncture sites) OR haematemesis OR melaena
Shock	Compensated: Capillary refill ≥ 3 sec or temperature gradient (leg); Decompensated: SBP < 70 mm Hg (children) or < 80 mm Hg (adults) + signs of impaired perfusion
Hyperparasitaemia	P. falciparum parasitaemia > 10%

Table1. Diagnostic criteria for severe malaria.

Data collection

A data collection form was drawn up. Data were collected from patients’ records. A detailed history and a clinical examination were recorded for each patient (age, sex, chief complaint, history of present illness, history, family history, personal history, treatment history, and the presence of risk factors). On admission, routine hematological investigations, plasma glucose tests, liver function tests, renal function tests, serum electrolytes, and malarial parasite tests (malaria rapid diagnostic tests (RDT), quantitative buffy coat, microscopy examination of thick blood films (METBF)) were performed.

Statistical analysis

Data analysis was carried out with SPSS (Statistical Package for Social Sciences) version 21 software. The descriptive study was carried out with the calculation of frequencies and proportions for the qualitative variables and the calculation of the means and standard deviations for the quantitative variables. The analytical study was done with cross tables. To compare the frequencies, we used the Pearson chi-square test or the bilateral Fisher exact test depending on their conditions of applicability; the comparison of the means was made with the analysis of variance test with a threshold of significance of p < 0.05. In multivariable analysis, binomial logistic regression with the stepwise method was used. This method consists of eliminating non-significant variables one by one in the model. It should be noted that only variables with a bivariate p-value of less than 25% were taken into account. The significance threshold used in this work is p < 0.05.

 

Results

During the study period, we collected 321 cases (Figure 1). There were 158 patients with AKI, representing a prevalence of 49.2%. The mean age was 36.25 years (12 and 86 years). The study population comprised 244 (76.0%) men and 77 (24.0%) women, giving a sex ratio of 3.14. The median length of hospital stay was 11 days (IQR, 1-14). Hypertension and diabetes mellitus were the most common comorbidities, with prevalence of 9.6% and 4.3%, respectively. Anuria was present in 64.3% of cases, oliguria in 26.8%, and edema in 7.14% (Table 2). Among patients with AKI, 88 (55.7 %) had pre-renal kidney failure, and 70 (44.3%) had AKI due to acute tubular injury. The KDIGO prognostic classification of AKI in our patients showed stage 1 in 34%, stage 2 in 25 %, and stage 3 in 41% of cases (Figure 2). RDT was performed in 258 patients and was positive in 249. METBF were carried out in 277 patients and were positive in 247 in patients. The Quantitative Buffy Coat (QBC) was performed on 3 patients and was positive in all cases.

For the entire cohort, mean blood urea was 1.2 g/L ± 2.6 and mean creatinine was 34.7 mg/L ± 40.1. For patients with AKI, mean blood urea was 2.1 g/L ± 2.3 and mean creatinine was 60.2 mg/L ± 48.1. Hyponatremia was noted in six patients, four of whom developed AKI. Hyperkalemia was noted in 25 patients, all of whom developed AKI. Artesunate was used for all patients. Rehydration was performed in 96.8% of cases. Hemodialysis was performed in 19 patients, with an average of 1.89 sessions. The indications for hemodialysis were hyperkalemia (12 patients), followed by uremic encephalopathy (10 patients) and pulmonary edema (2 patients). There were 5.3 % of patients who required invasive mechanical ventilation and 12.5% to high-flow nasal oxygen. The median non-renal SOFA score of all patients was 2 (IQR, 1–3). Patients with AKI exhibited a significantly higher non-renal SOFA score than patients with no AKI (3 [IQR, 2–4] vs 1 [IQR, 0–1]). Death occurred in 41 (12.77 %) patients, 78 % with AKI. Among patients with AKI, 111 (70.25 %) had complete remission of renal function and 12 (7.59%) had partial remission of renal function before leaving the hospital.  For patients who were on dialysis, nine had complete remission of renal function and two had partial remission of renal function before leaving the hospital. In univariable analysis, the risk factor significantly associated with the occurrence of AKI was herbal medicine (p = 0.029), hypertension  (p = 0.051); diabetes mellitus (p = 0.014); respiratoiry distress (p = 0.011); anemia (p = 0.001). In multivariate analysis, AKI-associated factors were herbal medicine (p = 0.045 [OR = 1.509; IC95%: [0.513-4.439]), diabetes mellitus (p = 0.044 [OR = 3.375; IC95%: [0.850-13.393]), respiratory distress (p = 0.034; OR = 2.758; IC95%: [0.907-8.389]) and anemia (p = 0.002; OR = 0.407; IC95%: [0.232-0.713]) (Table 3). In univariable analysis, risk factors significantly associated with the occurrence of death were Thrombopenia (p = 0,0001), respiratory distress (p = 0,0001) ; anemia (p = 0,049) ; leukocytosis (p = 0,018) ; AKI (p = 0,001). In multivariable analysis, the factors associated with death were gender (p = 0,0022; OR = 2,790; IC95%: [1,160-6,710]), respiratory distress (p = 0,047; OR = 2,745; IC95%: [0,863-8,735]); leukocytosis (p = 0,024; OR = 2,582; IC95%: [1,135-5,871]); thrombopenia (p = 0,004; OR = 0,098; IC95%: [0,020-0,476]); AKI (p = 0,004; OR = 3,584; IC95%: [1,467-8,754]) (Table 4).

Variables		All patients	AKI	No AKI	P value
Mean age (years)		36.25	36.3	36.1	0.926
Age > 60 years		49	27 (55.10%)	22 (44.90%)	0.371
Gender	Men	244	118 (48.36%)	126 (51.64%)	0.583
	Women	77	40 (51.95%)	37 (48.05%)
Herbal medicine		18	11 (61.10%)	7 (38.90%)	0.029
Smoking		45	22 (48.90%)	23 (51.10%)	0.962
Hypertension		31	17 (54.84%)	14 (45.16%)	0.051
Diabetes mellitus		14	4 (28.57%)	10 (71.43%)	0.014
Respiratory distress		21	16 (76.20%)	5 (23.80%)	0.011
Jaundice		119	64 (53.80%)	55 (46.20%)	0.210
RDT		249	130 (52.20%)	119 (47.80%)	0.838
Anemia		229	130 (56.80%)	99 (43.20%)	0.0001
Thrombocytopenia		235	114 (48.50%)	121 (51.50%)	0.674
Leukocytosis		153	97 (63.40%)	56 (36.60%)	0.0001

Table 2. Characteristics of the study population. RDT = Malaria rapid diagnostic tests.

Variables	Odds Ratio	95% CI	p value
Sex	1.002	[0.555-1.808]	0.996
Age > 60 years	1.878	[0.822-4.288]	0.013
Hypertension	0.703	[0.256-1.927]	0.493
Diabetes mellitus	3.375	[0.850-13.393]	0.044
Respiratory distress	2.758	[0.907-8.389]	0.034
Anemia	0.407	[0.232-0.713]	0.002
RDT	0.776	[0.429-1.404]	0.402
Leukocytosis	2.349	[1.485-3.715]	0.0001
Thrombocytopenia	1.114	[0.637-1.949]	0.706
Jaundice	1.292	[0.773-2.157]	0.328
Herbal medicine	1.509	[0.513-4.439]	0.045

Table 3. Factors associated with AKI (multivariable analysis). RDT = Malaria rapid diagnostic tests.

Variables	Odds Ratio	95% CI	p value
Age > 60 years	1.482	[0.455-4. 826]	0.514
Sex	2.79	[1.160-6. 710]	0.022
Hypertension	2.54	[0.414-15.576]	0.314
Diabetes mellitus	0.752	[0.074-7.623]	0.809
Respiratory distress	2.745	[0.863-8.735]	0.047
Anemia	0.731	[0.270-1.982]	0.539
RDT	3.560	[1.427-8.877]	0.006
Leukocytosis	2.582	[1.135-5.871]	0.024
Thrombocytopenia	0.098	[0.020-0.476]	0.004
Jaundice	0.733	[0.325-1.654]	0.455
Hyponatremia	0.735	[0.312-1.733]	0.482
Hyperkaliemia	0.148	[0.045-0.487]	0.002
Herbal medicine	0.859	[0.088-8.421]	0.896
AKI	3.584	[1.467-8.754]	0.004

Table 4. Factors associated with death for all patients (multivariable analysis). RDT= malaria rapid diagnostic tests; AKI = Acute kidney injury.

 

Discussion

In our study, the prevalence of AKI was 49.2%. The prevalence of AKI is variable in the literature. This variation in prevalence would be related to differences in socio-economic living conditions and the definition of AKI in the different studies. The World Health Organization (WHO) definition of renal impairment in severe malaria is a creatinine value >3mg/dl irrespective of patient age or baseline creatinine. This definition leads to substantial underestimation of AKI in patients with lower creatinine levels [6].  The 2023 WHO definition of AKI in severe malaria would therefore only detect stage 3 AKI; the stage at which AKI is present or imminent, and dialysis is often required for survival [7]. There are emerging data using consensus definitions to define AKI in severe malaria, reporting AKI in 24-59% of children hospitalized with severe malaria [8–12]. More recent data using the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines demonstrate that AKI is common in children hospitalized with malaria occurring in 19-59% of children with severe malaria [13].

Use of herbal medicine was a factor associated with AKI in our study. A systematic review of AKI in African children identified nephrotoxins in 16% of pediatric AKI [14]. Traditional herbal remedies or toxins can also contribute to AKI [14, 15]. In Africa, the population often resorts to traditional medicine due to the lack of doctors and healthcare facilities. Herbal medicine is not sufficiently studied in Africa and can lead to or worsen AKI.

In our study, anemia was associated with AKI. Anemia during severe malaria is caused by hemolysis. The primary contributors to hemolysis in malaria-endemic areas include P. falciparum infection, G6PD deficiency, sickle cell anemia, and other hemolytic anemias. Hemolysis-mediated kidney injury occurs due to increased oxidative stress, inflammation, endothelial dysfunction, and reduced nitric oxide bioavailability, all of which are implicated in severe malaria pathogenesis. Paracetamol represents a potential treatment to prevent AKI through its action as a potent inhibitor of hemoprotein-catalyzed lipid peroxidation (eg, cell-free hemoglobin, myoglobin) [16–18].

High levels of endogenous nephrotoxins, which are caused by haemolysis that releases cell-free haemoglobin and free heme, which are nephrotoxic and cause AKI through elevated oxidative stress [19, 20].

In our study, AKI was an independent factor of mortality. The identification of elevated blood urea nitrogen as a risk factor for prolonged hospitalization and neurologic deficits at discharge is novel in the context of malaria-associated AKI. AKI is a risk factor for long-term cognitive and behavioral problems [13] and disabilities [21]. AKI is a well-established risk factor for mortality in children with severe malaria and is associated with prolonged duration of hospitalization [8]. AKI is associated with increased post-discharge mortality in severe malaria [9]. Mortality would be higher in Low- and Middle-Income Countries (LMICs),  due to delayed diagnosis of malaria and especially of AKI. Human resources and equipment are not often available to allow for early diagnosis [1].  AKI screening markers such as serum creatinine (measured in the laboratory) are not always accessible in LMICs. Currently, we should focus more on tools that are more accessible and less expensive, such as urine dipsticks and point-of-care testing like creatinine meters [22]. Often, screening is only possible in urban areas where nephrologists can be found. A reorganization with decentralization is needed to improve screening methods. Primary health practitioners, nurses, and community personnel in remote areas must be trained to screen for AKI. The integration of community and rural personnel in the screening, diagnostic and therapeutic management of AKI can play an important role. The ISN 0by25 trial successfully demonstrated the utility of a symptom-based health assessment risk score coupled with a point of care creatinine and urine dipstick test in early recognition of kidney disease and appropriate triaging and management of patients presenting to primary healthcare centers in LMICs [23].The lack of adequate care also increases mortality. Today, even though antimalarials are much more accessible in Africa, there are still problems in managing severe malaria, particularly with renal involvement. Renal replacement therapies are not often accessible in LMICs. A systematic review showed that in sub-Saharan Africa, when dialysis was needed, the pooled dialysis access rate was 33% in adults and 64% in children [24]. The high cost of kidney replacement therapy (KRT) necessitates that LMICs strategize to improve accessibility for the general population. LMICs should take inspiration from Hong Kong’s example (71.9 % of the dialysis patients were on peritoneal dialysis (PD)) and resort to the least expensive KRT such as PD [25].

Programs like Saving Young Lives that promote acute PD, with local production of dialysate and bedside insertion of PD catheters, would make dialysis more accessible [26, 27].

The present study has some limitations. First, it was a retrospective cohort study, in which a high proportion of patients was lost during the long-term follow-up. The reliance of clinical adjudication to determine whether patients had acute tubular injury or prerenal azotemia increases the risk of patient misclassification.

 

Conclusion

AKI is common during severe malaria. It is associated with the severity of malaria, the presence of comorbidities and use of nephrotoxic products. AKI is independently associated with increased risk of death in severe malaria.

 

Acknowledgments

The authors wish to express their sincere gratitude to the Scientific Attaché at the Italian Embassy in Dakar, Dr. Eugenio Cavallo, for his invaluable support and for making this research possible through his commitment to fostering scientific collaboration and facilitating fieldwork activities in Senegal.

 

Bibliography

1. World Health Organization. World malaria report 2024. https://www.who.int/teams/global-malaria-programme/reports/world-malaria-report-2024
2. Randrianarisoa RMF, Ranivoharisoa EM, Ahmed M, Ramilitiana B, Rakotomalala NL, Randria MJ de D, et al. Acute kidney injury and severe malaria in adults: A monocentric descriptive study in Madagascar using KDIGO criteria. Nephrol Ther. 2021;17(6):434‑ https://doi.org/10.1016/j.nephro.2021.03.003.
3. Daher EF, da Silva GB Jr, Trivedi M, et al. Kidney complications of parasitic diseases. Nat Rev Nephrol 2022; 18: 396–406. https://doi.org/10.1038/s41581-022-00558-z.
4. World Health Organization. Guidelines for the Treatment of Malaria. 3rd edn. Geneva, Switzerland: WHO Press, 2015. https://iris.who.int/handle/10665/162441.
5. Kellum J, Lameire N, Aspelin P, et al. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl. 2012;2:1-138.
6. Batte A, Shahrin L, Claure-Del Granado R, Luyckx VA, Conroy AL. Infections and Acute Kidney Injury: A Global Perspective. Semin Nephrol. 2023 Sep;43(5):151466. https://doi.org/10.1016/j.semnephrol.2023.151466.
7. Batte A, Luyckx VA, Taylor TE, Conroy AL. Malaria guidelines fall short in diagnosing acute kidney injury. Lancet Glob Health. 2024 Feb;12(2):e194-e196. https://doi.org/10.1016/S2214-109X(23)00546-6. PMID: 38245108.
8. Conroy AL, Hawkes M, Elphinstone RE, et al. Acute kidney injury is common in pediatric severe malaria and is associated with increased mortality. Open Forum Infect Dis. 2016;3(2):ofw046. https://doi.org/10.1093/ofid/ofw046.
9. Conroy AL, Opoka RO, Bangirana P, et al. Acute kidney injury is associated with impaired cognition and chronic kidney disease in a prospective cohort of children with severe malaria. BMC Med. 2019;17(1):98. https://doi.org/10.1186/s12916-019-1332-7.
10. Oshomah-Bello EO, Esezobor CI, Solarin AU, Njokanma FO. Acute kidney injury in children with severe malaria is common and associated with adverse hospital outcomes. J Trop Pediatr. 2020;66(2):218–225. https://doi.org/10.1093/tropej/fmz057.
11. Afolayan FM, Adedoyin OT, Abdulkadir MB, et al. Acute kidney injuries in children with severe malaria: a comparative study of diagnostic criteria based on serum cystatin C and creatinine levels. Sultan Qaboos Univ Med J. 2020;20(4):e312–e317. https://doi.org/10.18295/squmj.2020.20.04.006.
12. Kunuanunua TS, Nsibu CN, Gini-Ehungu JL, et al. Acute renal failure and severe malaria in Congolese children living in Kinshasa, Democratic Republic of Congo. Nephrol Ther. 2013;9(3):160–165. https://doi.org/10.1016/j.nephro.2013.01.001.
13. Batte A, Berrens Z, Murphy K, et al. Malaria-Associated Acute Kidney Injury in African Children: Prevalence, Pathophysiology, Impact, and Management Challenges. Int J Nephrol Renovasc Dis. 2021;14:235–253. https://doi.org/10.2147/IJNRD.S239157 [PubMed: 34267538]
14. Olowu WA, Niang A, Osafo C, et al. Outcomes of acute kidney injury in children and adults in sub-Saharan Africa: a systematic review. Lancet Glob Health. 2016;4(4):e242–e250. https://doi.org/10.1016/S2214-109X(15)00322-8.
15. Evans RD, Hemmila U, Craik A, et al. Incidence, aetiology and outcome of community-acquired acute kidney injury in medical admissions in Malawi. BMC Nephrol. 2017;18(1):21. https://doi.org/10.1186/s12882-017-0446-4.
16. Plewes K, Kingston HWF, Ghose A, et al. Acetaminophen as a renoprotective adjunctive treatment in patients with severe and moderately severe falciparum malaria: a randomized, controlled, open-label trial. Clin Infect Dis. 2018;67(7):991–999. https://doi.org/10.1093/cid/ciy213.
17. Van Driest SL, Jooste EH, Shi Y, et al. Association between early postoperative acetaminophen exposure and acute kidney injury in pediatric patients undergoing cardiac surgery. JAMA Pediatr. 2018;172(7):655–663. https://doi.org/10.1001/jamapediatrics.2018.0614.
18. Desgrouas M, Boulain T. Paracetamol use and lowered risk of acute kidney injury in patients with rhabdomyolysis. J Nephrol. 2021. https://doi.org/10.1007/s40620-020-00950-7.
19. Plewes K, Kingston HWF, Ghose A, et al. Cell-free hemoglobin mediated oxidative stress is associated with acute kidney injury and renal replacement therapy in severe falciparum malaria: an observational study. BMC Infect Dis. 2017;17(1):313. https://doi.org/10.1186/s12879-017-2373-1.
20. Van Avondt K, Nur E, Zeerleder S. Mechanisms of haemolysis-induced kidney injury. Nat Rev Nephrol. 2019;15(11):671–692. https://doi.org/10.1038/s41581-019-0181-0.
21. Fitzgerald JC, Basu RK, Akcan-Arikan A, et al. Acute kidney injury in pediatric severe sepsis: an independent risk factor for death and new disability. Crit Care Med. 2016;44(12):2241–2250. https://doi.org/10.1097/ccm.0000000000002007.
22. Gama RM, Nebres D, Bramham K. Community Point of Care Testing in Diagnosing and Managing Chronic Kidney Disease. Diagnostics (Basel). 2024 Jul 17;14 (14):1542. https://doi.org/10.3390/diagnostics14141542.
23. Macedo E, Hemmila U, Sharma SK, et al; ISN 0by25 Trial Study Group. Recognition and management of community-acquired acute kidney injury in low-resource settings in the ISN 0by25 trial: A multi-country feasibility study. PLoS Med. 2021 Jan 14;18(1):e1003408. https://doi.org/10.1371/journal.pmed.1003408.
24. Olowu WA, Niang A, Osafo C, Ashuntantang G, Arogundade FA, Porter J, Naicker S, Luyckx VA. Outcomes of acute kidney injury in children and adults in sub-Saharan Africa: a systematic review. Lancet Glob Health. 2016 Apr;4(4):e242-50. https://doi.org/10.1016/S2214-109X(15)00322-8.
25. Li PK, Chow KM, Van de Luijtgaarden MW, Johnson DW, Jager KJ, Mehrotra R, et al. Changes in the worldwide epidemiology of peritoneal dialysis. Nat Rev Nephrol. 2017 Feb;13 (2):90-103. https://doi.org/10.1038/nrneph.2016.181.
26. Nkoy AB, Ndiyo YM, Matoka TT, et al. A promising pediatric peritoneal dialysis experience in a resource-limited setting with the support of saving young lives program. Perit Dial Int. 2020 Sep;40(5):504-508. https://doi.org/10.1177/0896860819887286.
27. Palmer D, Lawton WJ, Barrier C Jr, et al. Peritoneal Dialysis for AKI in Cameroon: Commercial vs Locally-Made Solutions. Perit Dial Int. 2018 Jul-Aug;38(4):246-250. https://doi.org/10.3747/pdi.2017.00190.