Thin-glomerular-basement-membrane (TGBM) nephropathy is among the most common causes of isolated hematuria. This autosomal dominant disorder is characterized by diffuse thinning of the GBM and is diagnosed by electron microscopic examination of renal biopsy tissue. A study of an affected kindred has revealed a mutation in the alpha chain of type IV collagen, resulting in abnormal basement membrane synthesis. Although the exact prevalence and prognosis is unclear, TGBM is usually regarded as a benign cause of hematuria and not associated with any untoward effect on renal function. We report a case of TGBM nephropathy, with associated proteinuria and progressive renal insufficiency. Other studies similarly contend that TGBM nephropathy may not be so benign. On the basis of these findings, we suggest that in some patients with TGBM nephropathy, progressive renal insufficiency may develop. We recommend a more vigilant approach in patients with TGBM nephropathy, especially if proteinuria is present.

We tested the hypothesis that a high concentration of serum ferritin, a frequently used marker of iron stores in dialysis patients and an acute-phase reactant, may be a marker of morbidity and mortality in these patients. To evaluate the impact of ferritin on morbidity and mortality, we reviewed the 6-month hospitalization rates in our dialysis patients retrospectively and subsequently reviewed the mortality among these patients over a 12-month period of time prospectively. One hundred one adult hemodialysis patients (59 men and 42 women; age, 54 +/- 15 years) who had been on hemodialysis for 38 +/- 27 months were studied. All but 5 patients were on intravenous iron with similar iron administration pattern. In the retrospective cohort, ferritin's correlation coefficients for hospitalization days and frequency (both r = +0.39, P: < 0.001) were higher compared with the albumin correlations for hospitalization days (r = -0.31, P: = 0.001) and frequency (r = -0.28, P: = 0.005) and correlation coefficients remained similarly significant after case-mix adjustment. In the prospective study, the "predeath" value of serum ferritin for 17 deceased patients (891 +/- 476 ng/mL) was higher than both their "initial" value (619 +/- 345 ng/mL, P: = 0.007) and the mean ferritin value of 84 surviving and withdrawing patients (639 +/- 358 ng/mL, P: = 0.001). Although Cox proportional hazard analysis showed a significant odds ratio of death only for serum albumin and not for ferritin, logistic regression analysis using the predeath values confirmed the significant impact of both decreased serum albumin and increased serum ferritin as markers of dialysis mortality. After case-mix adjustment, the relative risks of death for a 500 ng/dL increase in serum ferritin was 2.71 (95% confidence interval, 1.06 to 7.02) and for a 0.5 g/dL decrease in serum albumin was 4.48 (95% confidence interval, 1.77 to 11.33). Hence, serum ferritin is a strong predictor of hospitalization in dialysis patients. Although serum albumin is found to be a strong long-term marker of mortality in hemodialysis patients, an increase in serum ferritin appears to be a more reliable short-term marker of death over a 12-month period. Therefore, in the setting of uniform iron administration, a high serum ferritin may be a morbidity risk factor and a recent increase in serum ferritin may carry an increase in the risk of death in these patients.

Purpose of review

The novel corona virus (SARS-CoV2) has been demonstrated to cause acute kidney injury due to direct cellular toxicity as well as due to a variety of autoimmune glomerular diseases. The concept of a surge of infected patients resulting in an overwhelming number of critical patients has been a central concern in healthcare planning during the COVID-19 era.

Recent findings

One crucial question remains as to how to manage patients with end stage renal disease and acute kidney injury in case of a massive surge of critically ill infected patients. Some publications address practical and ingenious solutions for just such a surge of need for renal replacement therapy. We present a plan for using a blood pump, readily available dialysis filter, and a prefilter and postfilter replacement fluid set up. This is in conjunction with multiple intravenous pumps to develop a simple hemofiltration apparatus.

Summary

The current set up may be a readily available option for use in critical situations where the need for renal replacement therapy outstrips the capacity of traditional hemodialysis services in a hospital or region.

We evaluated an African American woman referred in 1986 at age 33 years because of renal potassium and calcium wasting and chronic hip pain. She presented normotensive, hypokalemic, hypocalcemic, normophosphatemic, and hypercalciuric. Marked hyperparathyroidism was evident. Urinary cyclic adenosine monophosphate (cAMP) excretion did not increase in response to parathyroid hormone (PTH) infusion, indicating renal resistance to PTH. X-rays and bone biopsy revealed severe osteitis fibrosa cystica, confirming skeletal responsiveness to PTH. Renal potassium wasting, suppressed plasma renin activity, and elevated plasma and urinary aldosterone levels accompanied her hypokalemia, suggesting primary hyperaldosteronism. Hypokalemia resolved with spironolactone and, when combined with dietary sodium restriction, urinary calcium excretion fell and hypocalcemia improved, in accord with the known positive association between sodium intake and calcium excretion. Calcitriol and oral calcium supplements did not suppress the chronic hyperparathyroidism nor did they reduce aldosterone levels. Over time, hyperparathyroid bone disease progressed with pathologic fractures and persistent pain. In 2004, PTH levels increased further in association with worsening chronic kidney disease. Eventually hypercalcemia and hypertension developed. Localizing studies in 2005 suggested a left inferior parathyroid tumor. After having consistently declined, the patient finally agreed to neck exploration in January 2009. Four hyperplastic parathyroid glands were removed, followed immediately by severe hypocalcemia, attributed to "hungry bone syndrome" and hypoparathyroidism, which required prolonged hospitalization, calcium infusions, and oral calcitriol. Although her bone pain resolved, hyperaldosteronism persisted.