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National strategies for addressing chronic kidney disease (CKD) are crucial to improving kidney health. We sought to describe country-level variations in non-communicable disease (NCD) strategies and CKD-specific policies across different regions and income levels worldwide. The International Society of Nephrology Global Kidney Health Atlas (GKHA) was a multinational cross-sectional survey conducted between July and October 2018. Responses from key opinion leaders in each country regarding national NCD strategies, the presence and scope of CKD-specific policies, and government recognition of CKD as a health priority were described overall and according to region and income level. 160 countries participated in the GKHA survey, comprising 97.8% of the world’s population. Seventy-four (47%) countries had an established national NCD strategy, and 53 (34%) countries reported the existence of CKD-specific policies, with substantial variation across regions and income levels. Where CKD-specific policies existed, non-dialysis CKD care was variably addressed. 79 (51%) countries identified government recognition of CKD as a health priority. Low- and low-middle income countries were less likely to have strategies and policies for addressing CKD and have governments which recognise it as a health priority. The existence of CKD-specific policies, and a national NCD strategy more broadly, varied substantially across different regions around the world but was overall suboptimal, with major discrepancies between the burden of CKD in many countries and governmental recognition of CKD as a health priority. Greater recognition of CKD within national health policy is critical to improving kidney healthcare globally.

Background Health information systems (HIS) are fundamental tools for the surveillance of health services, estimation of disease burden and prioritization of health resources. Several gaps in the availability of HIS for kidney disease were highlighted by the first iteration of the Global Kidney Health Atlas. Methods As part of its second iteration, the International Society of Nephrology conducted a cross-sectional global survey between July and October 2018 to explore the coverage and scope of HIS for kidney disease, with a focus on kidney replacement therapy (KRT). Results Out of a total of 182 invited countries, 154 countries responded to questions on HIS (85% response rate). KRT registries were available in almost all high-income countries, but few low-income countries, while registries for non-dialysis chronic kidney disease (CKD) or acute kidney injury (AKI) were rare. Registries in high-income countries tended to be national, in contrast to registries in low-income countries, which often operated at local or regional levels. Although cause of end-stage kidney disease, modality of KRT and source of kidney transplant donors were frequently reported, few countries collected data on patient-reported outcome measures and only half of low-income countries recorded process-based measures. Almost no countries had programs to detect AKI and practices to identify CKD-targeted individuals with diabetes, hypertension and cardiovascular disease, rather than members of high-risk ethnic groups. Conclusions These findings confirm significant heterogeneity in the global availability of HIS for kidney disease and highlight important gaps in their coverage and scope, especially in low-income countries and across the domains of AKI, non-dialysis CKD, patient-reported outcomes, process-based measures and quality indicators for KRT service delivery.

Rationale & Objective: Approximately 11% of people with kidney failure worldwide are treated with peritoneal dialysis (PD). This study examined PD use and practice patterns across the globe. Study Design: A cross-sectional survey. Setting & Participants: Stakeholders including clinicians, policy makers, and patient representatives in 182 countries convened by the International Society of Nephrology between July and September 2018. Outcomes: PD use, availability, accessibility, affordability, delivery, and reporting of quality outcome measures. Analytical Approach: Descriptive statistics. Results: Responses were received from 88% (n = 160) of countries and there were 313 participants (257 nephrologists [82%], 22 non-nephrologist physicians [7%], 6 other health professionals [2%], 17 administrators/policy makers/civil servants [5%], and 11 others [4%]). 85% (n = 156) of countries responded to questions about PD. Median PD use was 38.1 per million population. PD was not available in 30 of the 156 (19%) countries responding to PD-related questions, particularly in countries in Africa (20/41) and low-income countries (15/22). In 69% of countries, PD was the initial dialysis modality for ≤10% of patients with newly diagnosed kidney failure. Patients receiving PD were expected to pay 1% to 25% of treatment costs, and higher (>75%) copayments (out-of-pocket expenses incurred by patients) were more common in South Asia and low-income countries. Average exchange volumes were adequate (defined as 3-4 exchanges per day or the equivalent for automated PD) in 72% of countries. PD quality outcome monitoring and reporting were variable. Most countries did not measure patient-reported PD outcomes. Limitations: Low responses from policy makers; limited ability to provide more in-depth explanations underpinning outcomes from each country due to lack of granular data; lack of objective data. Conclusions: Large inter- and intraregional disparities exist in PD availability, accessibility, affordability, delivery, and reporting of quality outcome measures around the world, with the greatest gaps observed in Africa and South Asia.

IntroductionHypertension is a common public health problem and a key modifiable risk factor for cardiovascular (CV) and chronic kidney disease (CKD). Home blood pressure (BP) telemonitoring (HBPT) and management is associated with improved BP control, accelerated delivery of care and decision-making strategies that can reduce adverse outcomes associated with hypertension. The aim of this paper is to describe the protocol for a systematic review to assess the impact of HBPT interventions used for improving BP control and reducing CV and kidney outcomes in non-dialysis CKD patients.MethodsWe developed this protocol using the Preferred Reporting Items for Systematic reviews and Meta-Analyses for Protocols 2015. We will search empirical databases such as MEDLINE, Embase, Cochrane Library, CINAHL, Web of Science and PsycINFO and grey literature for studies conducted in non-dialysis CKD patients on interventions using HBPT and reporting outcomes related to BP control and other outcomes such as CV events and kidney disease progression. All studies meeting these criteria, in adults and published from inception until 2020 with no language barrier will be included.Ethics and disseminationEthical approval will not be required for this review as the data used will be extracted from already published studies with publicly accessible data. As this study will assess the impact of HBPT on BP control in non-dialysis CKD patients, evidence gathered through it will be disseminated using traditional approaches that includes open-access peer-reviewed publication, scientific presentations and a report. We will also disseminate our findings to appropriate government agencies.PROSPERO registration numberCRD42020190705).

Appropriate care in chronic renal insufficiency (CRI) includes blood pressure and diabetes control, as well as the investigation and management of anemia, acidosis, and bone disease. There is a lack of data on the control of these parameters at the time of referral to a nephrologist. Similarly, early referral has been emphasized in the literature, yet very little published has examined current referral patterns.A single-center retrospective/prospective review of all new outpatient referrals to nephrologists in Halifax, Canada, in 1998 and 1999 was conducted to identify patients with CRI (serum creatinine1.6 mg/dL [141 micromol/L] for men or1.2 mg/dL [106 micromol/L] for women). Quality of prereferral care was based on data from the initial clinic visit.Of 1,050 charts reviewed, 411 patients met the study criteria. Twenty-six percent of patients had diabetes mellitus, 18% were referred with a calculated glomerular filtration rate less than 15 mL/min, and blood pressure was optimally controlled (130 mm Hg systolic and80 mm Hg diastolic) in only 24%. Only 44% of patients were administered an angiotensin-converting enzyme inhibitor. Patients were administered an average of 1.9 antihypertensive agents. Significant anemia (hemoglobin10 g/dL) was present in 21%, and appropriate investigations were performed in only 35% of these patients. Calcium levels less than 8.6 mg/dL (2.15 mmol/L) were found in 19% of patients, and only 14% of these patients were started on calcium supplement therapy. Phosphate levels greater than 5.0 mg/dL (1.6 mmol/L) were seen in 20% of patients, and 14% of these patients were on phosphate-binder therapy. Parathyroid hormone levels were more than five times normal values in 18% of patients, and 25% of patients had bicarbonate levels less than 23 mmol/L.A significant proportion of patients referred with CRI receive inadequate prereferral care. Continuing education programs and referral guidelines must not only emphasize the importance of early referral, but also address the related consequences of CRI to delay the progression of renal disease and avoid complications.

Thirty-six patients on peritoneal dialysis (PD) for more than ten years in six North American centers were analyzed retrospectively. In the six centers, the percentage of patients surviving for more than ten years varied between 0.8% and 7.3%. The study group included 27 females and 9 males aged 38.6 ± 14.2 years [mean ± standard deviation (SD)] at the start of treatment. Of the 36 patients, 28 were Caucasian. The most common cause of end-stage renal disease (ESRD), present in 12 patients, was chronic glomerulonephritis. Only 4 patients had diabetes. At the beginning of the study, 19 patients had hypertension (the most common comorbid condition); 11 had no comorbid conditions at the start. Creatinine clearance at the start was 4.12 ± 3.5 mL per minute, and the mean duration to anuria was 51 ± 25 months. Mean initial body weight was 55 ± 9 kg, and mean body surface area was 1.5 ± 0.2 m2. Serum albumin levels showed an increase from 33.8 ± 3.6 g/L at the start of the study to 38.2 ± 3.9 g/L at the end. Hospitalization rate was low at 0.5 ± 0.3 admissions per patient–year, and duration of hospitalization was 4.8 ± 3.7 days per patient–year. Peritonitis was the most common cause of hospitalization. The mean peritonitis rate was 1 episode every 52 ± 48 patient–months. There were 36 catheter changes in 18 patients; 16 patients had a single PD catheter throughout the period of study. Autonomous hyperparathyroidism was the most common long-term complication. At the end of the study period, 11 patients were still on PD, 9 had died, 5 had been transferred to hemodialysis (HD), 1 was alive with a functioning allograft, and 1 was lost to follow-up. We conclude that patients who survive longer than ten years on PD are most likely to be young Caucasian females, small in body size, who are non diabetic, with few comorbid conditions. These long-term survivors have few hospitalizations, and their peritonitis rate is low. In this group of patients, severe autonomous hyperparathyroidism is the most common long-term complication.

Management of idiopathic crescentic and diffuse proliferative glomerulonephritis: Evidence-based recommendations. Idiopathic crescentic glomerulonephritis (GN) often presents with a rapid loss of renal function and pathology showing extensive crescent formation. The disease is caused by different immunopathogenetic mechanisms, pauci-immune, often antineutrophil cytoplasmic antibody (ANCA)-positive microvasculitis, anti-glomerular basement membrane (GBM) antibody disease, and immune complex formation. Historical reviews reveal poor renal prognosis, even after treatment with oral steroids and cytotoxic drugs. Prognosis has improved in the last decade. In this article, evidence-based recommendations for management are presented. Because of the high risk of end-stage renal disease (ESRD), early aggressive therapy is recommended, despite weak supporting evidence. Treatment for anti-GBM antibody-induced crescentic GN should be initiated early and should include pulse methylprednisolone, a two-week course of plasmapheresis and two months of treatment with corticosteroids and cyclophosphamide (grade B and C). Treatment for pauci-immune crescentic GN should be pulse methylprednisolone, followed by oral corticosteroids and cyclophosphamide for 6 to 12 months (grade B). Recurrences can be managed similarly (grade B), along with appropriate supportive therapy. In patients who develop ESRD, successful transplantation can be performed. Diffuse endocapillary proliferative GN is classically postinfectious. It generally has a good prognosis when no crescent formation occurs. Adult patients with persistent proteinuria, hypertension, and renal function impairment need careful follow-up and management to modify progressive hemodynamic injury.

Despite ongoing discussion of dialysis rationing in the nephrology community, there are little available data describing current practice in treatment selection for very ill renal patients with a poor prognosis. We report a prospective survey of end-stage renal patients referred to our Canadian regional dialysis center who were not accepted to the dialysis program on the grounds of poor prognosis and low quality of life. One quarter of patients referred during 1992 were not accepted to the program, with a mean age of 74 ± 11 years. Patients were predominantly female and most suffered from a combination of renovascular and cardiovascular disease, with very poor functional capacity as determined by the Karnofsky scale. Nonacceptance to the dialysis program did not create legal difficulties or requests for second opinions. Based on our experience, we propose guidelines for nonacceptance of patients to dialysis programs.

Prevention of hemodialysis subclavian vein catheter infections by topical povidone-iodine. Subclavian catheter (SCC) related infections are a major cause of morbidity in hemodialysis patients, the vast majority due to staphylococci species Povidone-iodine (PI) has proven anti-staphylococcal activity. Therefore, a randomized controlled trial of topical PI ointment was undertaken to evaluate the impact of this prophylactic intervention on the incidence of SCC related infections in hemodialysis patients. The role of S. aureus nasal carrier state in the acquisition of infection was also evaluated. Patients requiring SCC for temporary hemodialysis access were randomized to receive the treatment (T; N = 63) or sterile gauze dressings alone (C; N = 66). Catheter duration ranged from 2 to 210 days in both groups, with a mean of 38.6 days in T and 36.2 days in C (NS). Exit site (ES) infections were significantly less in T (5%) versus C (18%) (P < 0.02); tip colonization (TC) was 17% in T versus 36% in C (P < 0.01), while the incidence of septicemia (S) was also significantly less in C (2%) versus C (17%; P < 0.01). S. aureus nasal carriers were at a threefold higher risk of SCC related septicemia (0.009/day) than noncarriers (0.003/day; P < 0.05). The beneficial effect of PI ointment was most evident in this high risk group of S. aureus carriers: ES = 0% T versus 24% C, TC = 12% T versus 42% C, S = 0% T versus 29% C, P < 0.05. There were no adverse effects of the treatment. The routine application of topical PI ointment to temporary hemodialysis catheter exit sites is effective in reducing SCC related infections.

Objective To examine peritoneal dialysis technique survival in our regional, continuous ambulatory peritoneal dialysis (CAPD) program. Design Retrospective analysis. Setting Tertiary care dialysis programatan academic medical center. Patients 155 patients representing all those in the peritoneal dialysis program between October 1, 1987 and October 1,1990. Outcome measures The study analyzed patient and technique survival as well as the reasons for discontinuation of dialysis. In addition, the incidence and type of peritonitis and exit-site infection were also analyzed. Results Three-year actuarial patient survival was 66% and three-year technique survival was 86%, with data censored for death and transplant patients. Fiftyseven percent of transfers to hemodialysis were due to peritonitis, usually fungal or multiorganism bacterial. Only 1 patient failed due to exit-site and tunnel infection, and 1 due to inadequate dialysis. The catheter removal rate was 0.04 per patient-year. Conclusions Excellent CAPD technique survival can be achieved if exit-site and tunnel infection rates are low.

The high prevalence of cardiovascular disease in patients with kidney disease is well described. This Canadian, multi-centre, observational cohort study reports the prevalence and risk factors of CVD associated with kidney disease in a cohort of patients with established chronic kidney disease (CKD) who are followed by nephrologists. This analysis sought to answer 2 questions: (1) in patients with established CKD, are the prevalence and progression of CVD accounted for by conventional or uremia related risk factors? (2) to what extent can progression to RRT be explained by CVD versus ‘traditional risk factors’ for kidney disease?

A 22-year-old North American Indian prima gravida developed hypertension and edema at 28 weeks' gestation. A 24-hour urine collection contained 600 mg of protein, but no serum creatinine was measured. Despite bed rest and antihypertensive therapy with atenolol and a-methyl-DOPA, hypertension persisted. In addition, there were increases in transaminase levels. There was ultrasonographic evidence of intrauterine growth retardation, so delivery was made by cesarean section at 30 weeks' gestation of an 850-g male infant, who subsequently did well. Hypertension persisted postpartum to levels up to 210/120 mm Hg despite therapy with atenolol, 100 mg/d. Five weeks' postpartum, the patient complained of bilateral flank pain and edema. Serum creatinine was found to be 450 J.LmoJjL (normal

Objective To determine how effective angiotensinconverting enzyme (ACE) inhibitors must be in preventing diabetic nephropathy to warrant early and routine therapy in all Pima Indians with type 2 diabetes mellitus. Design A computerized medical decision analysis model was used to compare strategy 1, screening for microalbuminuria and treatment of incipient nephropathy as currently recommended with ACE inhibitor therapy, with strategy 2, a protocol wherein all patients were routinely administered an ACE inhibitor 1 year after diagnosis of type 2 diabetes mellitus. The model assumed that ACE inhibitors can block, at least in part, the pathogenic mechanisms responsible for early diabetic nephropathy (microalbuminuria). Results The model predicted that strategy 2 would produce more life-years at less cost than strategy 1, if routine drug therapy reduced the rate of development of microalbuminuria by 21% in all patients. Only a 9% reduction in the rate of development of microalbuminuria was cost-effective at $15,000 per additional life-year gained, and only a 2.4% reduction was cost-effective at $75,000 per additional life-year gained for strategy 2 over strategy 1. Conclusions Routine ACE inhibitor therapy in Pima Indians with type 2 diabetes mellitus could prove more effective and even cost saving than the currently recommended approach of microalbuminuria screening. A prospective trial examining this goal should be considered.

A 39-year-old woman became lethargic after working outside in her garden for several hours on a hot day. Over the next 10 days she became progressively more confused, ataxic, and was unable to look after her family. There was no history of vomiting, fever, chills, or use of medication. Her children claimed that she had taken some fluids in the form of fruit juice each day. Past history showed that 18 years before the current illness, the patient had required therapy for tuberculous meningitis. Of particular interest, at that time the patient was admitted with a stiff neck, seizures, and a serum sodium concentration of 113 mmollL (mEq/L). At the time of discharge, the serum sodium concentration was always higher than 150 mmol/L, and on one occasion reached 157 mmollL. She had not been ill since antituberculous therapy was completed, and no electrolytes had been checked until the current admission. When brought to the hospital by her husband, she was disheveled and incontinent, with a blood pressure of 80/60 mm Hg, and was disoriented and inappropriate. There were no localizing signs on neurologic examination. The admission laboratory data are given as day I in Table 1. Urine sodium and potassium levels were 128 and 102 mmollL, respectively. The patient was volume-repleted with 0.9% saline intravenously (IV) until her systolic blood pressure exceeded 100 mm Hg. Rehydration was then continued with 0.45% and 0.25 % saline. Urine output on the first day was approximately 700 mL. Despite gradual rehydration, the patient's mental status was slow to improve, and she was transferred to a university hospital 72 hours later. At that time she was normovolemic on examination, with a blood pressure of 120/80, no edema, and a jugular venous pressure 1 cm above the sternal angle. The laboratory data are reported as day 3 in Table I. The urine sodium and potassium were 284 and 20 mmollL, respectively, and the urine volume on that day was 1,800 mL. Because of ongoing confusion and failure of 0.9% saline infusions to raise the serum sodium level, the patient was treated with 1 Lid of 3 % saline IV for 3 days, and a fluid restriction. Serum electrolytes became normal, and the patient's mental state slowly returned to normal with no apparent residual damage in memory or cognitive function. The patient was then managed with a fluid restriction of 800 mLld, but due to a recurrence of hyponatremia (serum sodium, 132 mmollL, urine osmolality, 700 mOsm/L) therapy with demeclocycline, 300 mg twice daily, was instituted. On a prescribed daily fluid intake of 1.5 L, the serum sodium returned to normal, and urine osmolality averaged 450 mOsm/L. On day 21, the patient's serum sodium concentration was reported to be 158 mmollL, with a serum osmolality of 319 mOsm/L. The serum sodium concentration had been normal on day 16, and had risen gradually, but the patient was not thirsty. Review of her weight and fluid balance records from day 16 to 21 showed that the patient had a cumulative negative fluid balance of at least 3 L, because of her failure to ingest the prescribed fluid volume due to adipsia. Demeclocycline therapy was briefly withheld, oral fluids were given with closer nursing supervision, and the hypernatremia was corrected. Further investigation revealed no evidence of adrenal or thyroid insufficiency, nor of use of any drugs associ1tted with syndrome of inappropriate ADH secretion (SlADH). A computed tomography (CT) scan of the brain was initially normal, but a repeat study with contrast injection and analysis of coronal sections through the sella suggested the presence of a welldemarcated low-density lesion (but of higher density than cerebrospinal fluid) in the left hypothalamic area in association with the third ventricle.

The objective of this study was to determine how effective angiotensin- converting enzymes (ACEs) must be in preventing diabetic nephropathy to warrant routine administration to insulin-dependent diabetic patients. A Markov model was used to compare three strategies designed to prevent the development of end-stage renal disease in insulin-dependent diabetic patients. Strategy I, screening for microalbuminuria and treatment of incipient nephropathy as currently recommended, was compared with strategy II, a protocol in which patients were routinely administered an ACE inhibitor 5 years after diagnosis of diabetes, and strategy III, in which patients at high risk for nephropathy were routinely treated and low-risk patients followed a protocol in which patients were treated with an ACE inhibitor if they developed hypertension and/or macroproteinuria. The model predicted that strategy II would produce as many quality-adjusted life-years as strategy I at nearly the same cost if routine drug therapy reduced the rate of development of microalbuminuria by 26% in all patients. Strategy III produced as many quality-adjusted life-years at less cost than strategy I if a high-risk cohort could be identified with a rate of developing microalbuminuria at four times the rate of low-risk patients and if drug therapy reduced the rate of developing microalbuminuria in this high-risk group by 20%. In conclusion, routine ACE inhibitor therapy could prove to be cost-effective, especially if high-risk individuals could be identified. A prospective trial examining this goal should be considered. (Am J Kidney Dis 1998 Jan;31(1):49-54)

Chronic hemodialysis patients with failed native fistulas and/or synthetic arteriovenous grafts are usually dialyzed via surgically placed silicone jugular catheters such as the PermCath (Quinton, Seattle, WA, U.S.A.). We report a successful experience with the use of double lumen polyurethane central venous catheters placed percutaneously. Catheters with poor flows were replaced over a guidewire at the bedside. Eleven long-term hemodialysis patients failed arteriovenous access, 9 of them having had multiple attempts at fistulas and/or grafts. Seven of these patients had also failed peritoneal dialysis. They were dialyzed with polyurethane catheters for a mean of 681 +/- 280 days (range 282-1150 days), requiring a mean of 3.4 +/- 0.4 new venous punctures and 8.2 +/- 1.5 catheter changes over a guidewire over that period of time. Actuarial patient survival was 50% at 2 years, and mean urea reduction during dialysis was 64.2 +/- 1.7%. The septicemia rate was only 1.2 episodes per 1,000 catheter-days, but about 20% of patients experienced central venous occlusion, attributable to the use of subclavian catheter placement in 82% of the sites. The success of this technique and its elimination of the need for urokinase, radiologic interventions, and surgical placement warrant its consideration as an acceptable form of long-term vascular access, provided jugular placement allows reduced central venous occlusion rates.

The correction of uremic acidosis is one of the goals of hemodialysis; however, despite acceptable hemodialysis protocols, metabolic acidosis remains a common problem. The prevalence of acidosis and significance of factors affecting bicarbonate flux during hemodialysis were studied. A cohort of 70 stable patients receiving high-efficiency hemodialysis for at least 4 months was studied prospectively over a 1-year period. Twenty patients (28%) had a mean predialysis serum bicarbonate of less than 21 mEq/L. The patients with or without metabolic acidosis had similar mean net ultrafiltration and percent ultrafiltration, but acidotic patients had a higher percent increase in bicarbonate during hemodialysis (35 +/- 12 versus 27 +/- 10 [p = 0.008]). The latter suggests an increased net daily acid gain in patients with metabolic acidosis (1.19 +/- 0.32 mEq/kg versus 1.05 +/- 0.35 mEq/kg [p = 0.04]). A review of factors affecting intradialytic bicarbonate gain showed that predialysis serum bicarbonate (diffusive gradient) was the most significant with a demonstrated linear relationship between these two variables (R2 0.51). The role of dialysance and blood flow, assessed together using percent urea reduction, was minor as was the effect of ultrafiltration. At our level of dialysis delivery, prevalence of metabolic acidosis is low, and dialysis-related factors do not contribute to the persistence of metabolic acidosis. Net daily acid gain was higher in acidotic patients and accounts for the long-term maintenance of metabolic acidosis. For individual dialysis treatments, the diffusive gradient is the most important determinant of bicarbonate gain, with only a minor role being demonstrated for percent urea reduction and ultrafiltration rate.

BACKGROUND Iron deficiency is common in haemodialysis patients and adequate supplementation by the oral or parenteral route has been limited by drug side-effects, absorption, and cost. Intermittent doses of intravenous iron dextran complex are recommended in patients with inadequate iron stores despite maximal tolerated oral dose. We conducted a prospective study with economic analysis of a regular maintenance intravenous iron regimen in this group of patients. METHODS Fifty patients comprising one-half of our haemodialysis population required intravenous iron treatment, i.e. they failed to achieve an arbitrary goal serum ferritin 100 microg/l despite maximal tolerated oral iron dose. After a loading dose of intravenous iron dextran complex (IV-FeD) based on Van Wyck's nomogram (400+/-300 mg) they received a maintenance dose of 100mg IV-FeD once every 2 weeks. Initial goal serum ferritin was set at 100-200 microg/l. If no increase in haemoglobin was achieved at this level, transferrin saturation was measured to assess bioavailable iron, and when less than 20%, goal serum ferritin was increased to 200-300 microg/l. Recombinant human erythropoietin (rHuEpo) was used where needed to maintain haemoglobin in the 9.5-10.5 g/l range only if ferritin requirements were met. Results. Mean haemoglobin rose from 87.7+/-12.1 to 100.3+/-13.1 g/l (P

A 68-year-old white man was transferred from a regional hospital in Nova Scotia for further evaluation of severe hypoxia and pulmonary infiltrates. This man's illness started on April 18, 1993, when he woke up at night with pleuritic chest pain in the left inframammary area radiating to the left shoulder and left lateral chest. He was seen the following day by his family physician, who initially prescribed a muscle relaxant and subsequently an antibiotic, with no improvement in his symptoms. On the morning of May 13, his left-sided chest pain worsened and he became markedly short of breath. He had no cough, sputum, or hemoptysis and there were no fever, chills, or rigors. There was no history ofleg swelling or trauma to his legs. He smoked one pack of cigarettes per day for most of his life, but had recently reduced to a few cigarettes daily. His initial investigations revealed a white blood cell count of 11 .300 cells/ilL, hemoglobin 14.9 g/dL, POz 65 mm Hg on room air, and creatine phosphokinase 67 U/L. Chest x-ray film showed linear opacities in the bases bilaterally representing areas of atelectasis with probable superimposed infiltrate, and a ventilation-perfusion (V /Q) scan revealed a large perfusion defect in the anterolateral aspect of the left lung superiorly and a second one in the perihilar region of the same lung, as well as probable multiple smaller mismatched areas interpreted to indicate a high probability for pulmonary embolism. At this stage, the diagnosis of pulmonary embolism was made and he was started on heparin infusion, with the partial thromboplastin time adjusted to over twice the baseline. Subsequently. he developed further episodes of pain, intermittent low-grade fever, and hemoptysis, and the repeat V /Q scan reported slight adverse changes in the left upper lobe. He then underwent a bilateral lower limb radionuclide venogram that was negative for deep vein thrombosis. After a week of treatment with heparin. warfarin was introduced; when the patient's prothrombin time reached the therapeutic level, heparin was discontinued. On May 24, he started complaining of voiding difficulty and discoloration of his urine. Urine cultures were unremarkable, but he was noted to have proteinuria (0.3 gil) and hematuria (>250 red blood cellS/ilL) on urinalysis. On May 27, his chest pain worsened with deterioration of his oxygenation and he was sent to our institution for further evaluation of a pulmonary renal syndrome. At this time, a chest x-ray film revealed patchy peripheral air space opacification bilaterally, which was predominantly peripheral in location, with sparing of the apices and bases; he subsequently underwent a pulmonary angiogram that showed a marked decrease in flow to most of the left upper lobe and to the lateral aspects of the left lower lobe in association with attenuation of peripheral arteries and marked central pruning of some of the segmental branches in these regions. There were also a number of illdefined filling defects associated with these arteries, interpreted as late sequelae of extensive pulmonary emboli. There was mild renal insufficiency with creatinine 1.65 mg/dL; in addition, the above-mentioned urinary abnormalities persisted. Because a vasculitic process involving lungs and kidneys was suspected, the patient was started on pulse methylprednisolone and warfarin was discontinued. A nephrologic consultation was requested subsequently and a renal biopsy was performed on June 1 with no complications. Subsequently, the patient's condition deteriorated and he died on June 9, 1993, of respiratory failure.

A 36-year-old black man presented on a Friday evening with a I-week history of right-sided abdominal tenderness, chills, and dark urine. He had been treated by his family physician with oral tetracycline 100 mg once daily for 3 days, without benefit, and came to the hospital complaining of oliguria. Physical examination was not contributory, and urinalysis by a resident was reported as showing 3 giL of proteinuria, many red blood cells per high-power field, and several red blood cell casts. Serum creatinine was 314 /Lmol/L (3.6 mg/dL). There was a vague history of dark urine for a few days approximately 6 months earlier. A clinical diagnosis of rapidly progressive glomerulonephritis was made, with a concern that the lesion was superimposed on underlying 19A nephropathy, in view of the previous history of an episode of dark urine. Methyl prednisolone I g/d intravenously was administered for 3 days, and renal biopsy was planned for the following Monday. The serum creatinine increased to 750 /Lmol/L (8.5 mg/dL) and the potassium to 6.7 mmol/L. Hemodialysis three times weekly was initiated. Antineutrophil cytoplasmic antibodies were reported as absent, but on Monday morning the creatinine kinase was > 33,000 U/L (normal < 200 U/L). Hypocalcemia (1.23 mmol/L [4.93 mg/dL]) and hyperphosphatemia (5.28 mmol/ L [16.4 mg/dL]) were present. Myoglobin was detected in urine obtained 3 days after admission. Steroid therapy was discontinued. On further questioning, the patient admitted to some muscle tenderness and stiffness diffusely, but there was no weakness. The patient also confessed to drinking an unspecified volume of beer just before the illness started. Renal biopsy was obtained. Subsequently the patient's renal function returned to normal after 3 weeks of dialysis.

Long-term follow-up data are provided for a previously reported study of patients with membranous glomerulonephritis (MGN), nephrotic syndrome, and renal function impairment. Nine patients were treated with cyclophosphamide (1 to 2 mg/kg) and six of these received concurrent prednisone; they are compared with 17 concurrent controls (14 of whom had received prednisone at some time). The mean follow-up is 83 +/- 13 months in the treated patients and 64 +/- 7 months in the controls. Of the nine treated patients, four achieved a complete remission from the nephrotic syndrome (proteinuria less than 0.5 g/d), and five a partial remission (proteinuria decreased by at least 50% and to less than 3.5 g/d). One of the nine treated patients and 10 of the 17 controls have reached end-stage renal disease (ESRD) (P less than 0.05). Nine of the controls reaching ESRD had persistent nephrotic syndrome, whereas of the seven controls who have not yet reached ESRD, only two have persistent nephrotic syndrome (chi 2, P less than 0.02). There have been four relapses in three treated patients, and three of the four have responded to repeat therapy. One patient refused full therapy and remains nephrotic. Life-table analysis demonstrates significantly increased survival from ESRD in treated patients as compared with controls (P = 0.04).

A 37-year-old Caucasian male homosexual presented with hematuria and rapidly progressive acute renal failure. He was found to have proteinuria and microscopic hematuria as well as RBC casts. Investigations revealed polyclonal gammopathy with five times normal serum IgA levels as well as elevated serum IgG. Renal biopsy showed evidence of crescentic IgA nephropathy with ultrastructural changes of tubuloreticular inclusions described in HIV nephropathy. He was found to be positive for human immunodeficiency viral antibodies. Renal function improved during follow-up after two doses of 1 g each of methylprednisone. In our opinion, this is the first case of HIV-related crescentic IgA nephropathy. HIV testing should be performed more frequently in patients presenting with acute glomerular diseases.

A simple method to estimate the required dialysis time for cases of alcohol poisoning. Background Conventional dialysis management of ethylene glycol and methanol poisoning includes frequent intradialytic determinations of serum toxin concentration. Dialysis is continued until a target toxin concentration is reached. Initially, the required dialysis duration is unknown, making planning difficult. We devised a simple method to estimate the duration of dialysis required and avoid quantitation of multiple toxin samples. Methods Using the assumption that toxic alcohols would have a dialysis clearance similar to urea, we proposed that required dialysis time (hours) to reach a 5mmol/L toxin concentration target would be: [-V ln(5/A)]/0.06k, where V (liters) is the Watson estimate of total body water, A is the initial toxin concentration (mmol/L), and k is 80% of the manufacturer-specified dialyzer urea clearance (mL/min) at the initial observed blood flow rate. Directly measured dialysis and renal toxin clearance, and true dialysis requirement by conventional treatment protocol were compared with our estimate in two methanol and three ethylene glycol poisonings treated with Fresenius F8 dialyzers. Results There were no clinically or statistically significant differences between predicted dialysis duration (7.6 ± 1.9 hours, ±SD) and that actually provided using hourly toxin concentration sampling (7.4 ± 1.9 hours). Renal toxin clearance was negligible compared to that of dialysis, and predicted dialysis clearance did not differ significantly from that observed. Conclusions The simple estimate method is sufficiently valid to guide the prescription of dialysis for toxic alcohol poisoning. Data required at dialysis start include only the initial toxin concentration, dialyzer manufacturer's specified urea clearance at initial observed blood pump speed, and patient demographics to estimate total body water. This approach allows for planned dialysis therapy, without the need for additional toxin concentration measurements until dialysis is completed.

Patients with membranous glomerulonephritis (MGN), impaired renal function and the nephrotic syndrome are at high risk of developing renal failure. Twenty-six such patients were studied with serum creatinine concentrations exceeding 135 microM, and 24-hour urine protein excretion of at least 3.5 g/day to determine the potential benefit of cyclophosphamide therapy. Cyclophosphamide (mean 1.5 mg/kg/day) was given to nine patients for 23 +/- 4 months. These patients were compared with 17 concurrent controls. The two groups did not differ in clinical or laboratory features at the time of biopsy or start of treatment or its equivalent. Six of the nine cyclophosphamide treated patients and 15 of the 17 controls had received prednisone therapy. The total follow-up was 49 +/- 10 months in the treated group and 50 +/- 6 months in the controls. At last observation, serum creatinine values exceeded 400 microM in eight controls (4 on dialysis) and in none of the treated patients. The mean serum creatinine level was significantly lower (P less than 0.02) in the treated group (173 +/- 24 microM) than in controls (433 +/- 71 0.02) in the treated group (173 +/- 24 microM) than in controls (433 +/- 71 microM). The mean serum albumin level and 24-hour urine protein excretion both improved significantly with treatment as compared with controls. There were four complete remissions, five partial remissions and no patient with persistent nephrotic syndrome after treatment. In the controls, there were no complete remissions, six partial remissions and 11 patients had persistent nephrotic syndrome (P less than 0.001). Thus, cyclophosphamide therapy appears to be of benefit in patients with MGN, the nephrotic syndrome and impaired renal function.

The clearance characteristics of several commercially available high-flux dialyzers made from cellulose acetate, polyacrylonitrile, polysulphone, and polymethylmethacrylate were studied in vivo. The impact of increasing surface area and adding ultrafiltration on the clearances of small- and larger-molecular-weight species was assessed. The results show there are major differences in large-molecular-weight substance substance handling by different dialyzers as shown by differences in beta 2-microglobulin clearance, independent of ultrafiltration capacity. Membranes made from similar material, eg, Asahi's PAN and Hospal's AN-69 membrane, both made from polyacrylonitrile, differ significantly in their beta 2-microglobulin clearance. Increased surface area results in much greater increase in large-molecular-weight substance clearance. The present study clearly demonstrates that high water flux is not related to high large-molecular-weight permeability. Decisions with respect to impact on dialysis must be based on a knowledge of both the large- and small-molecular-weight permeabilities of the various membranes.