Pseudo-anion gap metabolic acidosis from severe hypertriglyceridemia corrected by plasma exchange
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BACKGROUND: Falsely low or even unmeasurable serum bicarbonate has been described in patients with severe hypertriglyceridemia or paraproteinemia. This phenomenon, known as pseudo-hypobicarbonatemia, is believed to be due to interference by these components when the commonly used enzymatic assay is utilized for serum bicarbonate measurement. The calculated bicarbonate derived from blood gas machines is not affected. This can lead to a misdiagnosis of a severe anion gap metabolic acidosis along with an extensive and expensive work-up. CASE PRESENTATIONS: We review a series of 5 patients with severe hypertriglyceridemia who presented with pseudo-hypobicarbonatemia and an elevated anion gap metabolic acidosis. Membrane-based therapeutic plasma exchange was utilized. RESULTS: Following aggressive lowering of the triglycerides, there was an immediate resolution of the pseudo-hypobicarbonatemia and anion gap metabolic acidosis. CONCLUSION: Recognition of lipemic serum in the setting of an otherwise unexplained anion gap metabolic acidosis should prompt the clinician to obtain a blood gas sample for true determination of the acid-base status. Doing so may avoid an extensive and expensive metabolic work-up.

Pathogenetic features of severe segmental lupus nephritis.

BACKGROUND: Accumulating evidence supports the notion that the pathogenesis of severe lupus glomerulonephritis is multifactorial and not solely an immune complex-mediated glomerular disease. Alternate mechanisms for glomerular destruction may exist. METHODS: We conducted a retrospective clinicopathologic analysis of 213 patients with lupus nephritis. Twenty-six patients had severe segmental glomerulonephritis (SSGN) and 15 patients had diffuse proliferative glomerulonephritis (DPGN). Patients with pure mesangial lupus nephritis [mesangial glomerulonephritis (MesGN)] (N = 13) were used as histologic controls. The degree of immunologic activity detailed by histologic data including light, fluorescent (IF) and electron microscopy (EM) on kidney biopsies and clinical data from patients with severe lupus nephritis were analysed. RESULTS: Biopsies from patients with SSGN had fewer glomeruli with wire loops (3 +/- 6% versus 35 +/- 34% P = 0.005) and hyaline thrombi (0.8 +/- 3% versus 16 +/- 22%, P = 0.02) compared to DPGN. The amount of IgG by IF was less in SSGN lesions compared to DPGN lesions, and IgG was absent in 30% of the SSGN group compared to none of the DPGN group (P = 0.04). There was no difference in mesangial deposits among the three groups (SSGN, DPGN and MesGN). The EM data supported the IF data. Anti-neutrophil cytoplasmic antibodies (ANCA) were essentially negative in all three groups and the C3 values tended to be lower in DPGN compared to SSGN (48 +/- 15 mg/dl versus 60 +/- 26 mg/dl, P = 0.09). CONCLUSIONS: The findings in DPGN involve a classic immune complex-mediated glomerulonephritis as demonstrated by the abundant immune aggregates witnessed in the peripheral capillary wall. In contrast, a paucity of peripheral immune aggregates is seen in SSGN implying a different pathogenesis. Our data support a mechanism of glomerular injury in SSGN that is separate from the generally accepted unitary concept of immune complex deposition in lupus nephritis.