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Objectives: We report our experience with posterior preperitoneal prosthetic hernioplasty for inguinal hernia in patients undergoing concomitant pelvic surgery for prostatic pathologies. Methods: 172 patients with unilateral or bilateral inguinal hernia underwent posterior preperitoneal prosthetic hernioplasty during pelvic surgery for BPH and malignant prostatic pathologies. Results: There was no evidence of hernial recurrence after a mean of 30 months and no complications attributable to the hernial repairs, except for 1 patient who developed a small periprosthetic hematoma and 1 patient with a pelvic lymphocele, both spontaneously resolved. Conclusions: Posterior preperitoneal prosthetic hernioplasty for inguinal hernia combined with pelvic surgery for prostatic pathologies should be applied routinely by urologists because it is a relatively simple procedure and with a very low rate of complications and recurrence.

A 38‐year‐old man begun to have paresthesias in the last three fingers of the left hand followed in few months by paresthesias in the right hand, weakness of distal muscles in upper limbs and paresthesias of lower limbs. HCV positivity was discovered by routine blood test. Neurological examination, 18 months after onset, showed asymmetric weakness and sensory loss with a nerve distribution more on the right side. Electrophysiological examination showed a sensory‐motor demyelinating neuropathy with motor conduction blocks and or excessive temporal dispersion of proximal compound muscle action potential in five nerves. Coexistence of focal motor and sensory conduction blocks at the same sites was demonstrated in three nerves. CSF examination showed increased protein content (66 mg/dl) and no cells. Cryoglobulins were absent. Active HCV‐RNA replication was detected in the serum by RT‐PCR. Liver biopsy revealed chronic hepatitis. Sural nerve biopsy showed fiber loss, prevalently of large diameter fibers, asymmetrical between fascicles and few clusters of regeneration. There were no demyelinating features, onion bulbs or inflammatory infiltrates. Weakness and electrophysiological findings worsened after high doses intravenous immunoglobulins but improved after intravenous methylprednisolone and interferon alpha treatment with resolution of conduction blocks in two months. Multifocal acquired demyelinating sensory and motor neuropathy (MADSAM), as in the patient we describe, is a rare disorder considered an asymmetric variant of chronic inflammatory demyelinating neuropathy (CIDP). HCV infection is usually associated with a multineuropathy due to vasculitis or a symmetric sensory‐motor axonal polyneuropathy. CIDP has been described but never MADSAM. It is difficult to be sure of a pathogenetic link between a dysimmune demyelinating neuropathy and HCV infection, nonetheless the coexistence of hepatitis makes the choice of treatment problematic in these patients.

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The association between CIDP and glomerulonephritis has been rarely reported: membranous glomerulonephritis in five cases, focal‐segmental glomerulosclerosis in two, IgA nephropathy in one. A pathogenetic autoantibody towards a common antigen in myelin and glomerular basement membrane has been hypothesized. A 60‐year‐old man developed proteinuria (3.4 g/24 h) without clinical signs of nephrotic syndrome and, six months later, paresthesias and progressive limb weakness. Examination showed ataxic gait, predominantly distal weakness with bilateral foot drop, glove‐stocking sensory loss, reduced or absent reflexes, and postural tremor. Electrophysiological studies revealed a sensory‐motor demyelinating polyneuropathy with marked axonal loss in lower limbs. CSF examination showed increased proteins. HBV, HCV and HIV markers, rheumatoid factor, ANA, ANCA, ENA were negative. Monoclonal gammopathy and cryoglobulins were absent. C3 and C4 were normal. Circulating immune complexes were 37% (n.v. <35). Anti‐ganglioside (GM1, GM2, GA1, GD1a, GD1b), anti‐ sulfatide, and anti‐MAG antibodies were negative. Sural nerve biopsy showed small epineurial and perineurial infiltrates, marked loss of fibers, and no deposits of IgG and IgM or amyloid. Kidney biopsy revealed a membranoproliferative glomerulonephritis with associated interstitial nephritis. Neurological and renal abnormalities improved with plasmaphereses and prednisone. This patient represents the first with the association between membranoproliferative glomerulonephritis and CIDP, and the sixth, to our knowledge presenting with CIDP and glomerulonephritis. Our results seem to exclude a common pathogenetic role of antiganglioside, anti‐MAG and antisulfatide antibodies in this case.