We report on two cases of acute liver injury along with the intake of Greater Celandine (Chelidonium majus), a well-known herbal remedy frequently used for irritable bowel syndrome. All other possible causes of acute liver damage were excluded in both patients. In one patient, cholestatic hepatitis recurred rapidly after involuntary re-exposition. Both patients fully recovered after the withdrawal of Greater Celandine. The two cases add to the existing database about the potential hepatotoxicity of drugs containing Greater Celandine and raise the question whether the approval of this drug should be re-evaluated in the light of lacking evidence for a therapeutic benefit.

Over a period of 68 months we observed 33 patients with biopsy-confirmed severe crescentic glomerulonephritis (GN) and another 5 patients who fulfilled the clinical criteria of rapidly progressive glomerulonephritis (RPGN; no biopsy confirmation) in a region comprising approximately 930,000 inhabitants. Additional 7 patients with Wegener’s granulomatosis (WG)/microscopic polyarteritis (MP) from the same region were not seen by nephrologists. The calculated annual incidence of crescentic GN/RPGN is 0.7/100,000. Of the 38 patients 13 had classical WG, 7 MP, 3 systemic lupus erythematosus, 5 Schönlein-Henoch purpura, 3 Goodpasture’s syndrome, 2 IgA glomerulonephritis. Of note is the high prevalence of WG/MP and the relative frequency of Schönlein-Henoch purpura. At the last follow-up, 3 patients were dead (8%), 7 patients were on dialysis (18%), 7 patients had elevated serum creatinine (18%) and 21 patients had normal serum creatinine (55%). We conclude that: (i) RPGN is more frequent than reported; (ii) WG and MP account for more than 50% of cases of RPGN; (iii) renal functional prognosis is good in WG/MP, but less favorable in RPGN of other causes; (iv) severe hypertension is not a feature of RPGN; (v) WG/MP, and not Goodpasture’s syndrome, is the most common cause of pulmonary hemorrhage in association with RPGN; (vi) death from infection or malignoma is uncommon (not observed in this series); (vii) de novo IgA GN may occur in patients in remission from WG (2 observations).

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A 17-year-old male presented with nephrotic syndrome associated with microscopic hematuria. Renal biopsy showed only minor glomerular abnormalities (light microscopy). Immunohistology demonstrated strong mesangial deposition of IgA. Electronmicroscopy disclosed widespread effacement of foot processes in combination with isolated osmiophilic mesangial deposits. The patient responded to standard corticosteroid therapy with complete disappearance of proteinuria. Microscopic hematuria, however, persisted. Five months after steroid therapy was stopped, the nephrotic syndrome relapsed. It was again steroid-responsive with persisting microhematuria. From clinical and morphological data we conclude that the patient has concomitant idiopathic nephrotic syndrome (minimal change glomerulonephritis) and mesangial IgA glomerulonephritis. The simultaneous presence of these two diseases may give some hint as to their pathogenesis. In both, abnormalities in T cell regulation have been found. If these were indeed involved in the pathogenesis of the two glomerular diseases, a higher than expected probability for the two entities to coexist in the same patient is to be expected.